Cell Recognition & The Immune System

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Cell Recognition

Specific molecules on the surface of cells and viral particles allow the body to identify them as self or non-self.
These molecules are usually proteins on the phospholipid bilayer, such as glycoproteins, but glycolipids can also act as markers.
Surface proteins enable recognition of pathogenic cells, abnormal body cells (e.g. cancerous or infected), toxins, and cells from other individuals of the same species.
In organ transplants, the body must not recognise the donated organ as foreign to avoid an immune response.

Antigens

Antigens are unique markers (macromolecules) found on cell membranes, bacterial walls, or viral surfaces.
Glycolipids and glycoproteins on membranes often act as antigens.
Antigens enable cell-to-cell recognition and help distinguish between self and non-self.
Self antigens are produced by the body’s own cells and do not trigger an immune response.
Non-self antigens are large molecules on foreign cells (e.g. pathogens, incompatible blood cells) that stimulate an immune response.
Some pathogens (e.g. cold and flu viruses) show antigen variability due to frequent genetic mutations, changing their surface antigens.
Antigen variability means existing lymphocytes and memory cells can no longer bind (no complementary receptors), preventing a secondary immune response and allowing reinfection.

Phagocytosis

Phagocytes are white blood cells produced continuously in the bone marrow; the two main types are neutrophils and macrophages.
Phagocytosis is a non-specific immune response where phagocytes recognise and engulf pathogens.
Chemotaxis: chemicals from pathogens or damaged cells (e.g. histamines) attract phagocytes to the infection site.
Recognition and attachment: phagocytes detect non-self antigens using receptor proteins, which bind to antigens on the pathogen.
Engulfment: the phagocyte membrane extends around the pathogen, forming a phagocytic vacuole (endocytosis).
Phagosome formation: the vacuole containing the pathogen is now called a phagosome.
Phagolysosome formation: the phagosome fuses with a lysosome, forming a phagolysosome.
Digestion: lysozymes (digestive enzymes) hydrolyse the pathogen (e.g. breaking down bacterial cell walls).
Antigen presentation: in macrophages, digested pathogen fragments may be displayed on the cell surface to activate the specific immune response.

The T Lymphocyte Response

Lymphocytes are white blood cells involved in the specific immune response; they are smaller than phagocytes, have a large nucleus, and are produced in bone marrow before birth.
T-lymphocytes (T cells) target and destroy abnormal or infected body cells – the cellular response.
B-lymphocytes (B cells) produce antibodies that target antigens in body fluids – the humoral response.
Antigen-presenting cells are host cells invaded by a pathogen that display the antigen on their surface membrane using major histocompatibility complexes (MHCs).
T helper cells are activated when they bind to their specific antigen on an antigen-presenting cell; they then divide by mitosis to form clones.
Activated helper T cells release cytokines, which stimulate maturation of B-lymphocytes into antibody-secreting plasma cells, production of memory B and T cells, enhanced phagocytosis, and activation of cytotoxic T cells.
Cytotoxic T cells (T killer cells) patrol for infected cells displaying foreign antigens; they bind and release toxic substances (e.g. perforins) to destroy the infected cells.

The B Lymphocyte Response

Each mature B lymphocyte has a specific antibody on its surface that acts as a receptor.
Clonal selection occurs when a B cell binds to a complementary antigen.
The activated B cell divides by mitosis (clonal expansion) into plasma cells (secrete large amounts of antibodies) and memory cells (provide a faster secondary response).
The immune response involving B lymphocytes and antibody production is called the humoral response.
B cells can be activated by antigens binding directly to antibody receptors or by antigen-presenting cells binding to antibody receptors.
The primary immune response is slow because it takes time to make enough antibodies.
By the time a child is born, it has millions of different types of B-lymphocytes, each with a specific antibody receptor.

Antibodies

Antibodies are globular glycoproteins with a quaternary structure, shaped like a Y.
They are made of 2 heavy and 2 light polypeptide chains, joined by disulfide bonds.
Each chain has a constant region (same for antibodies within one class; determines destruction method) and a variable region (different in each antibody; forms the antigen-binding site).
The antigen-binding site is specific to a particular region on the antigen called the epitope.
Specificity comes from differences in the amino acid sequence of the variable region.
A hinge region (not present in all classes) gives flexibility to bind antigens at different angles.
When an antibody binds to a complementary antigen, they form an antigen-antibody complex.
Y-shaped antibodies have two antigen-binding sites, so they can bind to more than one antigen, causing agglutination (clumping of pathogens).
Binding of antibodies either neutralises the pathogen or acts as a marker to attract phagocytes, which engulf and destroy the pathogens.

Plasma & Memory Cells

During an immune response, B-lymphocytes give rise to plasma cells (produce antibodies) and memory cells (basis of immunological memory).
Primary immune response: after clonal selection and mitosis, plasma cells secrete specific antibodies; these cells are short-lived and antibody numbers gradually decrease.
Some B-lymphocytes develop into memory cells that remain in the blood for a long time.
The primary response is slow due to time taken for clonal selection, mitosis, and antibody production.
Secondary immune response: if the same antigen is encountered again, memory cells recognise it and divide very quickly into plasma cells.
The secondary response is quicker and produces more antibodies than the primary response.
If memory cells are present, infections can be destroyed before symptoms develop.
Immunological memory explains why catching some diseases twice is unlikely, but antigenic variability (e.g. cold, flu) means the primary response must occur each time.

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Übungsfragen

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1.Which type of molecule most commonly acts as an antigen on the surface of a cell?
Easy
- AGlycoprotein
- BPhospholipid
- CStarch
- DCellulose
2.Which statement best defines a non-self antigen?
Easy
- AA large molecule found on a foreign cell that stimulates an immune response
- BA molecule produced by the body's own cells that does not trigger an immune response
- CA chemical released by helper T cells to stimulate B cells
- DA digestive enzyme released by a lysosome to hydrolyse pathogens
3.Self antigens produced by the body's own cells trigger an immune response.
Easy
True or false?
4.Which of the following are results of cytokines released by helper T cells? (select all that apply)
Medium
- AMaturation of B lymphocytes into antibody-secreting plasma cells
- BProduction of memory B and T cells
- CAn enhanced rate of phagocytosis
- DActivation of cytotoxic T cells
- EDirect secretion of antibodies by helper T cells
5.Where are T lymphocytes matured?
Medium
- AIn the thymus gland
- BIn the bone marrow
- CIn the spleen
- DIn the lymph nodes
6.Match each cell or molecule with its correct description.
Medium
- Plasma cell
- Memory cell
- Cytotoxic T cell
- Antibody
- Secretes large amounts of antibodies
- Remains in the blood to provide a faster secondary response
- Releases toxic substances to destroy infected cells
- Globular glycoprotein that binds complementary antigens
7.Why can a person catch the common cold more than once?
Medium
- ACold viruses show antigen variability, so existing memory cells have no complementary receptors
- BMemory cells destroy the virus too quickly to produce symptoms
- CThe common cold is caused by bacteria that are not recognised as non-self
- DAntibodies against cold viruses are broken down before they can act
8.Which part of an antibody is specific to one antigen?
Medium
- AThe variable region, which forms the antigen-binding site
- BThe constant region, which determines the destruction method
- CThe disulfide bonds joining the chains
- DThe hinge region in the heavy chain

Mehr Fragen

9.Place the stages of phagocytosis in the correct order.
Medium
- Chemotaxis attracts the phagocyte to the infection site
- Receptors bind to antigens on the pathogen surface
- The membrane extends around the pathogen forming a phagocytic vacuole
- The phagosome fuses with a lysosome
- Lysozymes hydrolyse the pathogen
10.Why is the primary immune response relatively slow?
Medium
- AIt takes time for clonal selection, mitosis and antibody production to occur
- BPlasma cells are long-lived and release antibodies slowly
- CMemory cells must be produced before any antibodies can be made
- DAntibodies must be broken down before they can bind antigens
11.The secondary immune response produces more antibodies more quickly than the primary immune response.
Easy
True or false?
12.Which of the following are classified as non-self antigens? (select all that apply)
Medium
- AGlycoproteins on the surface of an incompatible donor red blood cell
- BMolecules on the surface of a virus particle
- CGlycoproteins on the membrane of a healthy body cell
- DMolecules on the surface of a bacterial cell wall
- EGlycolipids on the membrane of the body's own liver cell
13.Which of the following are roles of cytokines released by helper T cells? (select all that apply)
Medium
- AStimulating maturation of B lymphocytes into antibody-secreting plasma cells
- BDirectly engulfing pathogens by phagocytosis
- CActivating cytotoxic T cells
- DProducing memory B and T cells
- ECreating holes in infected cell membranes using perforins
14.Which of the following statements about phagocytes are correct? (select all that apply)
Easy
- APhagocytes are produced continuously in the bone marrow.
- BPhagocytosis is an example of a specific immune response.
- CNeutrophils and macrophages are two main types of phagocyte.
- DPhagocytes only recognise self antigens.
- EPhagocytes detect non-self antigens using receptor proteins on their membrane.
15.Match each stage of phagocytosis with its correct description.
Medium
- Chemotaxis
- Engulfment
- Phagosome formation
- Phagolysosome formation
- Digestion
- The vacuole containing the pathogen is now called a phagosome.
- Chemicals from pathogens or damaged cells attract phagocytes to the infection site.
- Lysozymes are released to hydrolyse the pathogen.
- The phagocyte's membrane extends around the pathogen, forming a phagocytic vacuole.
- The phagosome fuses with a lysosome.
16.Match each antibody structure with its correct description.
Medium
- Heavy polypeptide chain
- Light polypeptide chain
- Constant region
- Variable region
- Hinge region
- Different in each antibody and forms the antigen-binding site.
- Gives flexibility to bind antigens at different angles.
- Same for antibodies within one class and determines the destruction method.
- One of the two longer chains in an antibody molecule.
- One of the two shorter chains in an antibody molecule.
17.Place the stages of the specific immune response involving B lymphocytes in the correct order.
Medium
- Clonal selection
- Clonal expansion
- Differentiation into plasma cells and memory cells
- Antibody secretion by plasma cells
- Memory cells provide long-term immunity
18.Place the events of the cellular immune response in the correct order.
Medium
- Antigen-presenting cell displays antigen on its surface
- Helper T cell binds to its specific antigen
- Helper T cell divides by mitosis to form clones
- Cytokines are released
- Cytotoxic T cells are activated
19.Antibodies are globular glycoproteins with a quaternary structure shaped like a Y.
Easy
True or false?
20.Cytotoxic T cells release cytokines to activate B cells.
Easy
True or false?
21.Antigen variability allows some pathogens to avoid a secondary immune response because their surface antigens change.
Medium
True or false?
22.A person may develop the common cold twice within a short time. Which statement best explains why?
Medium
- AThe common cold is caused by many different virus strains with different antigens, so memory cells from the first infection are not complementary to the new strain.
- BThe immune system produces antibodies that are too specific and cannot recognise any virus.
- CMemory cells are short-lived and die within a few days.
- DThe common cold virus does not trigger an immune response.
23.Which of the following best describes the role of antigen-presenting cells?
Medium
- ATo activate specific T cells that have complementary receptors to the antigen
- BTo produce antibodies against pathogens
- CTo directly engulf and destroy pathogens by phagocytosis
- DTo release perforins to kill infected cells
24.Plasma cells contain many mitochondria and an extensive endoplasmic reticulum. Which statement best explains why these features are important adaptations?
Medium
- AMitochondria provide ATP for antibody synthesis, and the endoplasmic reticulum packages and transports antibodies.
- BMitochondria store antibodies, and the endoplasmic reticulum provides energy for cell division.
- CMitochondria produce antibodies, and the endoplasmic reticulum destroys pathogens.
- DMitochondria and endoplasmic reticulum are both involved in phagocytosis of pathogens.
25.A person recovered from an influenza infection, and their blood was found to contain influenza antibodies 6 months later. Explain why this patient was able to catch influenza again several days after their blood tested positive for flu antibodies.
Hard
- AThe influenza virus mutates frequently, changing its surface antigens so existing memory cells are no longer complementary.
- BThe antibodies against influenza are short-lived and disappear within days.
- CThe patient's memory cells were destroyed by the influenza virus.
- DThe patient had not produced any memory cells during the first infection.
26.A patient is given a kidney transplant. Before the transplant, doctors check that the donor kidney's surface antigens match the patient's. Which statement best explains why this matching is important?
Medium
- AIf the antigens are recognised as non-self, the patient's immune system may destroy the donated kidney.
- BIf the antigens are recognised as self, the patient's immune system will destroy the donated kidney.
- CMatching antigens ensures the donor kidney produces the same antibodies as the patient.
- DMatching antigens prevents the donor kidney from producing non-self antigens after surgery.
27.A phagocyte engulfs a bacterium. Which of the following events occur during this process? (select all that apply)
Medium
- AThe phagocyte's membrane extends around the bacterium to form a phagocytic vacuole.
- BThe phagosome fuses with a lysosome to form a phagolysosome.
- CLysozymes hydrolyse the bacterial cell wall.
- DAntibodies are secreted by the phagocyte to neutralise the bacterium.
- EThe bacterium is killed by perforins released from the phagocyte.
28.Agglutination occurs because antibodies have two antigen-binding sites, allowing them to clump pathogens together.
Easy
True or false?
29.Match each component of an antibody with its correct description.
Medium
- Variable region
- Constant region
- Hinge region
- Forms the antigen-binding site and is specific to one antigen
- Same for antibodies within one class and determines the destruction method
- Gives flexibility to bind antigens at different angles
30.Place the stages of the cellular immune response in the correct order.
Medium
- Antigen-presenting cell displays antigen on MHC
- Helper T cell with complementary receptor binds to antigen
- Helper T cell divides by mitosis to form clones
- Cytokines activate cytotoxic T cells
- Cytotoxic T cells release perforins to destroy infected cells
31.A patient has a blood transfusion. Their blood group is A, and they are given blood group B. Which statement best explains why this is dangerous?
Hard
- AThe patient's anti-B antibodies will bind to the B antigens on the donated red blood cells, causing agglutination.
- BThe donated blood's anti-A antibodies will bind to the patient's A antigens, causing agglutination.
- CThe patient's B antigens will bind to the donated blood's anti-B antibodies, causing agglutination.
- DThe donated B antigens are recognised as self by the patient's immune system, causing an immune response.
32.During phagocytosis, the phagosome fuses with a lysosome to form a phagolysosome. Which statement best explains why this fusion is essential for the destruction of a pathogen?
Medium
- AIt allows lysozymes to be released so that the pathogen is hydrolysed.
- BIt allows the pathogen to be presented on the cell surface membrane.
- CIt allows the phagocyte to produce antibodies against the pathogen.
- DIt allows the pathogen to be recognised as non-self by receptor proteins.
33.In an investigation, a student placed phagocytes into a well containing a suspension of bacteria. They counted the number of bacteria remaining in the suspension at intervals over 30 minutes. Which change to the investigation would be most likely to increase the rate at which the bacteria are removed from the suspension?
Medium
- AIncubating the well at 10 °C instead of 37 °C.
- BAdding a chemical that prevents the phagocytes from carrying out endocytosis.
- CIncreasing the concentration of bacteria in the suspension.
- DAdding a chemical that attracts phagocytes towards the bacteria.
34.A scientist is investigating the response of T lymphocytes to a viral infection. Which of the following observations would provide evidence that clonal selection has occurred? (select all that apply)
Hard
- AA specific T lymphocyte binds to a complementary antigen presented on a macrophage.
- BThe number of T lymphocytes with a particular receptor increases rapidly.
- CCytokines are released by helper T cells.
- DA T lymphocyte divides by mitosis to produce genetically identical cells.
- EAll T lymphocytes in the body respond to the same antigen.
35.A student made a slide of a blood smear and observed it under a light microscope. They identified a cell with a large nucleus that filled most of the cell, and very little cytoplasm. Which type of cell did they most likely observe?
Medium
- AA neutrophil
- BA macrophage
- CA lymphocyte
- DA plasma cell
36.In an antigen-presenting cell, antigens are displayed on major histocompatibility complexes (MHCs) on the cell surface membrane.
Easy
True or false?
37.Match each stage of phagocytosis with the correct description.
Medium
- Chemotaxis
- Engulfment
- Phagolysosome formation
- Antigen presentation
- Phagocyte membrane extends around the pathogen, forming a phagocytic vacuole.
- Chemicals from pathogens attract phagocytes to the infection site.
- Digested pathogen fragments are displayed on the cell surface membrane.
- The phagosome fuses with a lysosome.
38.Place the following events of the T lymphocyte response in the correct order.
Medium
- A macrophage presents a pathogen antigen on its cell surface membrane.
- A helper T cell with a complementary receptor binds to the antigen.
- The helper T cell divides by mitosis to form clones.
- Cytokines are released, stimulating B cells and cytotoxic T cells.
- Cytotoxic T cells release perforins to destroy infected cells.
39.A scientist investigated the effect of an antibody on a bacterial culture. They mixed bacteria with antibodies and observed that the bacteria clumped together. They then added phagocytes and found that the bacteria were destroyed more quickly than when phagocytes were added to bacteria without antibodies. Which statement best explains these observations?
Hard
- AAntibodies directly hydrolyse the bacterial cell walls, making the bacteria easier to destroy.
- BAntibodies neutralise the bacteria by blocking their surface antigens, preventing them from moving.
- CAntibodies cause agglutination, allowing phagocytes to engulf many bacteria at once, and act as markers to attract phagocytes.
- DAntibodies stimulate the bacteria to produce antigens that are more easily recognised by phagocytes.
40.Which of the following is a correct definition of an antigen?
Easy
- AA protein produced by plasma cells that binds to pathogens
- BA molecule on the surface of a cell that enables cell recognition and can stimulate an immune response
- CA chemical released by helper T cells that activates B cells
- DAn enzyme that hydrolyses bacterial cell walls
41.Name the process by which a phagocyte engulfs a pathogen.
Easy
42.Complete the sentence about antibody structure.
Easy
Antibodies are made of two ____ polypeptide chains and two light polypeptide chains, joined by disulfide bonds.
43.Name the cells that remain in the blood after an infection and provide long-term immunity.
Medium
44.Name the process by which antibodies cause pathogens to clump together.
Medium
45.State the part of an antigen that binds to an antibody.
Easy
46.How many polypeptide chains make up one antibody molecule?
Medium
47.Complete the sentence about the secondary immune response.
Medium
The secondary immune response is ____ and produces ____ antibodies than the primary immune response.
48.An antibody molecule is made of heavy and light polypeptide chains. How many polypeptide chains make up one antibody molecule?
Medium
49.Name the part of an antigen that binds to the antibody.
Medium
50.Name the specific region of an antigen that binds to an antibody.
Easy
51.How many antigen-binding sites does a single Y-shaped antibody molecule have?
Medium
52.Complete the sentence about antigen variability using the words provided.
Medium
Some pathogens show antigen variability because of frequent genetic ____. Their surface antigens change, so existing ____ and memory cells can no longer bind due to there being no ____ receptors.
53.Describe how phagocytosis occurs when a rhinovirus enters the human body.
Medium
54.Explain how structure A (the variable region) in an antibody ensures that the antibody will only detect one specific antigen.
Hard
55.Explain how the structure of an antibody ensures that it will only bind to one specific antigen.
Hard
56.Define the term antigen.
Medium
57.Explain why a person can catch the common cold more than once.
Hard
58.How many polypeptide chains make up one antibody molecule?
Medium
- A3
- B5
- C6
- D4
59.An antibody molecule is made of heavy and light polypeptide chains. How many polypeptide chains make up one antibody molecule?
Medium
- A3 chains
- B4 chains
- C6 chains
- D5 chains
60.How many antigen-binding sites does a single Y-shaped antibody molecule have?
Medium
- A2
- B4
- C1
- D3

Lernnotizen

## Cell Recognition & The Immune System **Cell recognition** – specific surface molecules (usually glycoproteins/glycolipids on the phospholipid bilayer) let the body distinguish **self** from **non-self**. This identifies pathogens, abnormal (e.g. cancerous) cells, toxins, and cells from other individuals. **Antigens** – macromolecules on cell membranes, bacterial walls or viral surfaces (often glycolipids/glycoproteins) that enable cell-to-cell recognition. - **Self antigens** – produced by own cells; do **not** trigger an immune response. - **Non-self antigens** – on foreign cells (pathogens, incompatible blood); **stimulate** an immune response. - **Antigen variability** – pathogens (cold/flu) mutate, changing surface antigens; existing lymphocytes/memory cells have no complementary receptors, so no secondary response → reinfection. Explains why flu vaccines are updated. ## Phagocytosis (non-specific) Phagocytes (neutrophils, macrophages) made in bone marrow. Sequence: 1. **Chemotaxis** – chemicals (e.g. histamines) attract phagocytes. 2. **Recognition/attachment** – receptors bind non-self antigens. 3. **Engulfment** – membrane extends around pathogen forming a phagocytic vacuole (endocytosis). 4. **Phagosome** formation. 5. **Phagolysosome** – phagosome fuses with lysosome. 6. **Digestion** – lysozymes hydrolyse the pathogen. 7. **Antigen presentation** – fragments displayed on cell surface (macrophages) to activate specific response. ## T Lymphocyte (cellular) response - **Antigen-presenting cells** display antigens on **MHCs**; activate complementary T cells. - **Helper T cells** bind specific antigen → divide by mitosis → release **cytokines**, which stimulate: maturation of B-lymphocytes into antibody-secreting plasma cells; production of memory B and T cells; enhanced phagocytosis; activation of cytotoxic T cells. - **Cytotoxic (T killer) cells** bind infected cells and release toxic substances; **perforins** make holes in the membrane. ## B Lymphocyte (humoral) response - Each mature B cell has a specific surface antibody receptor. - **Clonal selection** – B cell binds complementary antigen (directly or via antigen-presenting cell). - **Clonal expansion** – divides by mitosis into **plasma cells** (secrete antibodies) and **memory cells**. - **Primary response** is slow (time for selection, mitosis, antibody production). - **Secondary response** – memory cells recognise antigen, divide quickly → **faster**, **more** antibodies. ## Antibodies - Globular **glycoproteins**, Y-shaped, **quaternary** structure; 2 heavy + 2 light chains joined by disulfide bonds. - **Constant region** – same within a class; determines destruction method. - **Variable region** – forms the **antigen-binding site**, specific to the **epitope**; specificity from amino acid sequence. - **Hinge region** – flexibility. - **Antigen-antibody complex** forms when complementary shapes bind. Two binding sites → **agglutination** (clumping); pathogens can't move easily → phagocytes engulf many at once. Binding neutralises pathogen or marks it for phagocytes. ## Plasma & Memory Cells - **Plasma cells** – short-lived, secrete specific antibodies; numbers fall after response. - **Memory cells** – remain in blood long-term → immunological memory. - **Primary**: slow, fewer antibodies. **Secondary**: quicker, more antibodies; can destroy infection before symptoms. **Key contrast:** clonal **selection** = activation by complementary antigen; clonal **expansion** = mitosis producing identical cells.

Antigen: A macromolecule (often glycolipid/glycoprotein) on a cell membrane, bacterial wall or viral surface that enables cell recognition; non-self antigens stimulate an immune response.
Self antigen: Antigen produced by the body's own cells that does not trigger an immune response.
Non-self antigen: Large molecule on a foreign cell (e.g. pathogen, incompatible blood cell) that stimulates an immune response.
Antigen variability: Frequent genetic mutations change a pathogen's surface antigens, so existing lymphocytes and memory cells can no longer bind (no complementary receptors), preventing a secondary immune response.
Phagocytosis: Non-specific immune response in which phagocytes recognise and engulf pathogens.
Chemotaxis: Movement of phagocytes towards chemicals (e.g. histamines) released by pathogens or damaged cells.
Phagosome: The vacuole containing an engulfed pathogen.
Phagolysosome: Structure formed when a phagosome fuses with a lysosome.
Lysozymes: Digestive enzymes released to hydrolyse pathogens (e.g. breaking down bacterial cell walls).
Antigen presentation: Display of digested pathogen fragments on the cell surface (e.g. by macrophages) to activate the specific immune response.
Antigen-presenting cell: A host cell invaded by a pathogen that displays the antigen on its surface membrane via MHCs.
MHC (major histocompatibility complex): Structure on which antigen-presenting cells display antigens to activate specific T cells.
Helper T cells: T cells activated by binding their specific antigen on an antigen-presenting cell; divide by mitosis and release cytokines.
Cytokines: Chemical signals released by helper T cells that stimulate B-lymphocyte maturation into plasma cells, memory B and T cell production, enhanced phagocytosis, and cytotoxic T cell activation.
Cytotoxic (T killer) cells: T cells that patrol for infected cells displaying foreign antigens, bind to them and release toxic substances (perforins) to destroy them.
Perforins: Substances released by cytotoxic T cells that create holes in the membrane, allowing toxins to enter and kill the cell.
Clonal selection: The process where a specific B or T lymphocyte is activated after binding to a complementary antigen.
Clonal expansion: The process where the selected lymphocyte divides by mitosis to produce a large number of identical cells.
Plasma cells: Short-lived cells formed from activated B cells that secrete large amounts of specific monoclonal antibodies.
Memory cells: Cells that remain in the blood long-term and provide a faster, stronger secondary immune response.
Humoral response: The immune response involving B lymphocytes and the production of antibodies.
Cellular response: The immune response in which T-lymphocytes target and destroy abnormal or infected body cells.
Antibody: A globular glycoprotein with a quaternary structure, made of 2 heavy and 2 light polypeptide chains joined by disulfide bonds.
Constant region: Part of an antibody chain that is the same for antibodies within one class; determines the destruction method.
Variable region: Part of an antibody chain that differs in each antibody and forms the antigen-binding site.
Epitope: The part of the antigen that binds to the antibody.
Hinge region: Region in the heavy polypeptide chain (not present in all classes) that gives flexibility to bind antigens at different angles.
Antigen-antibody complex: Formed when an antibody binds a complementary antigen; binding neutralises the pathogen or marks it for phagocytes.
Agglutination: Clumping of pathogens caused by antibodies binding more than one antigen at a time; clumped pathogens cannot move easily and are engulfed by phagocytes.
Primary immune response: Slow response to a newly encountered antigen, involving clonal selection, mitosis and antibody production.
Secondary immune response: Quicker response producing more antibodies, due to memory cells recognising a previously encountered antigen.

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