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1 There are two forms of immunity: innate and adaptive.

2 Innate immunity is broad and immune responses are rapid (minutes to hours).

3 Unlike adaptive immunity, innate immunity does not exhibit memory to antigenic exposure.

4 Many elements participate in innate immunity, including various physical barriers (e.g., skin), chemical barriers (e.g., low pH in stomach), cellular components (e.g., phagocytes, neutrophils, NKT cells), germline‐encoded pattern recognition receptors (e.g., TLRs, NLRs), and complement.

5 Alterations in expression of chemokine receptors and adhesion molecules facilitate the recruitment of immune cells to sites of injury.

6 Macrophages and neutrophils of the innate immune system facilitate destruction of invading organisms by upregulating phagolysosome activity and cytokine secretion.

7 When innate immune defense mechanisms fail to completely eliminate invading pathogens, defense mechanisms mediated by adaptive immune cells (B and T lymphocytes) are called into play and this process is facilitated by innate immune cells which play major roles in antigen presentation and cytokine activation of these cells.

8 Complement refers to a set of >50 serum proteins that cooperate with both innate and adaptive immune systems to eliminate pathogens. Its major roles include opsonization of microbes, recruitment of phagocytes to sites of infection, and, in some cases, direct killing of microbes as a result of the terminal stages of complement activation that can form the lysis‐promoting membrane attack complex.

9 The three major pathways of complement activation are: (a) the classic pathway initiated when C1q binds to antigen–antibody complexes; (b) the lectin pathway in which complement’s mannose‐binding lectin binds to conserved carbohydrates on pathogens; and (c) the alternate pathway involves direct binding of C3 to certain microbial surfaces such as LPS. C3 also undergoes constitutive spontaneous hydrolysis in solution at a low level and binds to host cell surfaces. The presence of inhibitory regulatory molecules in mammalian cells prevents damage to such cells. Because microbes lack these regulatory proteins, the binding of C3 to their surface initiates the cascade of complement activation that results in lysis of the microbe.