Immune responses are normally stimulated responses produced when an individual is exposed to a foreign antigen.
Types of Immune response:
A. According to kinetics:
1. Primary immune response: The immune response that occurs on the first exposure to a foreign material in the body is called primary immune response.
2. Secondary immune response: The immune response which is a much quicker and more effectible than the primary immune response & occur after previously encountered antigen reappears is called secondary immune response.
B. According to mechanism of action:
1. Humoral immune response: Mediated by the secreted molecules present in the body fluids (humors).
2. Cellular immune response: Mediated by activated T-lymphocytes.
primary immune response: The immune response that occurs on the first exposure to a foreign material in the body is called primary immune response.
Characteristics of primary immune response:
• Longer lag period.
• Higher levels of specific IgM and lower level of IgG produced.
• Steady state level persists for short time.
• IgM predominates.
Secondary immune response: The immune response which is a much quicker and more effective than the primary immune response & occurs after a previously encountered antigen reappears is called secondary immune response.
Characteristics of Secondary immune response:
• Shorter lag period.
• Lower levels of IgM and higher levels of IgG produced or IgG predominates.
• Steady state level persists longer.
• Quantitative difference between primary and secondary immune response due to increase in the number of potentially reactive B-0cells
Antigen presentation by helper T-cells:
A. Exogenous antigens presentation:
These exogenous antigens enter antigen presenting cells or APCs (macrophages, dendritic cells and B-lymphocytes) Through phagocytosis . The microbes are engulfed and placed in a phagosome. After lysosomes fuse with the phagosome, protein antigens are degraded by proteases into a series of peptides. These peptides eventually bind to grooves in MHC-ll molecules and are transported to the surface of the APCs. T4-lymhocytes are then able to recognize peptide/MHC-ll complexes by means of their T-cell receptors (TCRs) and CD4 molecules.
Steps of exogenous antigen presentation:
1. Exogenous antigen, such as viruses, are engulfed and placed in a phagosome.
2. Lysosomes fuse with the phagosome forming a phagolysosome.
3. Protein antigens are degraded into a series of peptides.
4. MHC-ll molecules are synthesized in the endoplasmic reticulum and transported to the golgi complex. Once assembled, within the endoplasmic reticulum, a protein called the invariant chain attaches to the peptide-binding groove of the MHC-ll molecules and in this way prevents peptides designated for binding to MHC-l molecules with the RR from attaching to the MHC-ll.
5. The MHC-ll molecules with bound li chain are now transported to he Gogi compes and placed in vesicles.
6. The vesicles containing the MHC-ll molecules fuse with the peptide-containing phaglysosomes. The li chain is removed and the peptides are now free to bind to the grooves of the MHC-0ll molecules.
7. The MHC-ll molecules with bound peptides are transported to the cytoplasmic membrane where they become anchored. Here, The peptide and MHC-ll complexes can be recognized by T4 lymphocytes by way of TCRs and CD4 molecules having a complementary shape.
8. After recognition of TCRs and CD4 molecules represents the first signal necessary for activation of the t4 lymphocyte .Co-stimulatory signals involving the interaction of costimulatory molecules such as CD40 and B7 molecules on the APC with their correspondiding ligands on the T4 lymphocyte are also nevessary for avtivation. Thes co-stimulatory molecules are only synthesized when toll-like receptors on APCs bind to pathogen associalted moleclular patterns of microbes. Without the interaction of the costimulatory molecules the T4 lymphocyte si not activated and undergoes apoptosis.
B. Edogenous antigenspresenttion
The body marks infected cells and tumor cells for destruction by placing peptide epitopes from these endogenous antigens on their surface by way of MHC-l molecules. Cytotoxic T-lymphocytes (CTLs) are then able to recognize peptide 4HC-l complexes by means of their T-cell receptors (TCR) and CD8 molecules and kill the cells to which they bind.
Steps of endogenous antigens presentation:
1. Endogenous antigens, such as viruses, are engulfed and placed in a phagosome.
2. Lysosomes fuse with the phagosome forming a phagolysosome.
3. Endogenous antigens, such as viral proteins, pass through proteasomes where they are degraded into a series of peptides.
4. The peptides are transported into the rough endoplasmic reticulum (ER) by a transporter associated protein or TAP.
5. The peptides then bind to the grooves of newly synthesized MHC=l molecules.
6. The endoplasmic reticulum transports the MHC-l molecules with bound peptides to the Golgi complex.
7. The Golgi complex, in turn, transports the MHC-l peptide complexes by way of an exocytic vesicle to the cytoplasmic membrane where they become anchored.
Role of Cd4 or helper T-lymphocytes (TH) in immune response:
1. Regulatory cells play a central role in the immune response.
2. Once primed by APC presentation of antigen, They
• Stimulate to proliferation of other T-cells by chemically or directly.
• Stimulate B-cells that have already become bound to antigen.
3. Without TH, there is no immune response.
4. TH cells interact directly with B-cells that have antigen fragments on their surfaces bound to MHC-ll receptors.
5. TH cells stimulate B-cells to divide more rapidly and begin antibody formation.
6. B-cells may be activated with TH cells by binding to T-cell independent antigens.
7. Most antigens, however, require TH co-stimulation to activate B-lymphocytes.
8. Cytokines released by TH amplify nonspecific defenses
9. Helper T-lymphocytes:
• Secretes interleukins.
• Coordinate humoral and cellular immunity.
Kinetics of the immune response:
There are qualitative and quantitative differences in the antibody production at various times of immune response. The first exposure of an individual to a particular antigen is referred to as the priming events and the measurable response is celled the primary response and second & subsequent exposure to the same antigen is known as secondary response. Antibody response can be divided into 4 different phases namely lag phase, log phases, phase of plateau and phase of decline.
1. Lag phase: After initial contact with an antigen, a considerable period of time is elapsed before antibody is detectable in the serum. The length of time is generally 1-2 weeks, depending on the species immunized and the type of adjuvant used. The latent period included the time taken for B-cells to make contact with the antigen, to proliferate, to differentiate and then to secrete antibody in quantity sufficient enough to be detected in the serum.
2. Log phase: During this phase, the concentration of antibody in the serum increases exponentially.
3. Plateau: A constant antibody level is maintained in the serum for some times. It indicates a critical balance between the production and removal of antibody from the body.
4. Phase of decline: During this phase serum antibody level declines due to the clearing of antigen-antibody complexes and natural catabolism of the immunoglobulins.
Factor influencing primary and secondary immune response:
The type and magnitude of immune response depends on the following factors:
1. Nature of antigen.
2. Doses of antigen.
3. Route of entry of antigen.
4. Genetic makeup of the host.
5. Previous exposure to antigen.
Homeomodulation 