1)
Pathogen |
Non-pathogen |
Opportunistic pathogen |
Organisms that causes infection or disease. |
Organisms that do not cause infections or diseases |
Organisms that cause disease in individual under immunocompromised conditions |
When a pathogen or infectious agent enters the body and colonizes within the body, it results in metabolic, physiological, or structural changes. These changes cause to clinical manifestations or symptoms. |
These organisms may enter the body or may be part of common flora. The act as commensals, may also be benefitial |
These organisms may not cause disease in healthy individual. However, in immunocompromised individual the organisms cause disease as host defense mechanism is weak. |
Example: Salmonella typhi causes typhoid |
Example- Lactobacillus sp. can be used as food supplements |
Example: Mycoses causing fungi like Candida, Cryptococcus, Trichophyton, Histoplasma, Blastomyces, affecting AIIDs patient. |
2)
3)
Immune response is initiated when,the body encounters any foreign molecules acting as exogenous or endogenous antigens). The innate immunity or non-specific immunity acts as the first line of defense, provides barrier against the foreign substances.
Various cytokines released from specific cells, like interleukins (IL), tumor necrosis factor alpha (TNFα), activates the production of mature phagocytic cells, like neutrophils, macrophages and dendritic cells and induce their migration to the site of infection or invasion.
Phagocytic cells, engulf the foreign substances by phagocytosis or endocytosis.
The phagocytosed molecules processed and, then the peptide fragments of antigens are expressed through membrane bound glycoproteins called major histocompatibility complex (MHC).
The antigenic polypeptide bound to MHC molecules further induces B-lymphocytes (designated from Bursa of Fabricus in birds) and T-lymphocytes (lymphocytes maturing in thymus), generating humoral or cell mediated immune responses, as well as immunogenic memory. Such specific activations lead to clonal selection, clonal expansion and clonal deletion.
a) Activation of helper T-lymphocytes(TH): They are mediators for the activation of both humoral or cell mediated immune responses. The naïve TH cells, with T-cell receptor- cluster of differentiation 3 complexes (TCR CD3), reacts to class II MHC molecules associated with antigenic polypeptide. This induces other T-cell surface receptors like CD28, leading to further interactions with MHCII-polypeptide complexes. The TH cells then proliferates and differentiates into memory cells and effector cells or mature cells with CD4receptors. TH cells are subdivided into TH1 (activating B-cells), TH 2 (activating T-cytotoxic cells) and other subtypes, which secretes different cytokines, that induces other immune cells. TH cells also mediate clonal anargy.
b) Activation of B-lymphocytes- B- cells may be activated, by direct interactions with TH cells, and are called response to thymus-dependent (TD) antigens, or may be activated without direct contacts with TH cells, by thymus-independent antigens.These two types of signals may activate naïve B-cellsdifferentiates into memory B-cells and effector B cells (or plasma cells). Plasma cells release antibodies. Antibodies, released to the plasma, tissue fluid and lymph, contribute to humoral immunity.
c) T cytotoxic cells (TC)CD 8 receptors on T cytotoxic cells recognizes type I MHC molecules bound antigenic peptides, and co-stimulatory responses. They contribute to the cell mediate immunity. TC, then differentiates into memory cells ad effector cells called cytotoxic T-lymphocytes (CTLs). CTLs then further recognizes MHC-I complexes bound to the target cell, and thus destroy the target cell.
4)
Immune system can distinguish between self and non-self-antigens, failure to which may cause fatal consequences.
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