The cells which take part in adaptive immunity are T cells. B cells and monocyte - Macrophage system.
Treg cells are a subgroup of CD4 + T cells used to prevent autoimmune responses. Mechanism used by Treg cells to down regulate inflammation is the production of the anti-inflammatory cytokine IL - 10.
The elevation in body temperature in fever is due to resetting of the hypothalamic set point mediated by cytokines.
The term "complement" was introduced by Paul Ehrilich. Complements account for 5% of the globulin fraction of blood serum and can serve as opsinins. C3b can act as opsonins. "Terminal" componenets (C5b, C6, C7, C8 and C9) is called as membrane attack complex. C5a, act as chemoattractants for PMNs.
The host receptor for P. Vivax is Duffy Fy antigen. Receptor for P. Falciparum is Glycophorin A and the receptor for Entamoeba histolytica is N-Acetyl glucosamine [APPG-1-2014]
Rabies virus grows in striated muscle cells at the site of inoculation.
H1-subtype strains of influenza bind to a receptor composed of two sugar molecules: sialic aced linked alfa-2-6 to galactose. This is highly expressed in the airway epithelium. (Since it attaches to the upper airway, it spreads commonly but it is mild).
H5N1 avian influenza virus binds to sialic acid linked alfa-2-3 to galactose, and this receptor is highly expressed in pneumocytes in the alveloli. This leds to high mortality rate and also the low human-to-human transmissibility rate.
Most capsules are carbohydrates, exception is B. anthracis, which contains polypeptide capsule.
LPS from gram negative bacteria attaches with GPI anchored membrane protein - CD14 on the surface of phagocytes.
Toll-like receptors (TLRs) are expressed in macrophages and dendritic cells, that recognize microbes. TLRs initiate cellular activation through nuclear factor kappa B (NF-kB), a master - switch for production of inflammatory cytokines. Bacterial flagella binds to TLR5. Pathogens that do not bind to TLR5 are Campylobacter jejuni, Helicobacter pylori, and Bartonella bacilliformis.
Inflammasome are the site where inflammatory cytokines IL-1beta and IL-18 are changed from their precursor to active forms prior to secretion by the cysteineprotease caspase-1. Four inflammasomes with different components are formed: the IPAF inflammasome, the NALP1 inflammasome, the cryoprin/NALP3 inflammasome, and an inflammasome triggered by Francisella tularensis infection.
Adenovirus inhibits host defense by decreasing production of major histocompatibility complex molecules. Epstein-Barr virus and cytomegalovirus inhibits host defense by diminishing cytotoxic T cell recognition of virus-infected cells.
Organisms that act by inhibiting ADP-ribotransferase activity are cholera, Diphtheria Pertussis, E.Coli - heat labile toxin and P. Aeuroginosa exotoxin (A, S and T). Pseudomonas inject toxins directly into host Target cells by means of a complex set of proteins leading to stimulation of Type III system.