1. Defense against extracellular pathogens

2. Defence against extracellular pathogens  bacteria (gram-negative, gram-positive cocci, bacilli), unicellular parasites  complement activation stimulated by bacterial cell wall  phagocytosis by neutrophil granulocytes  opsonization (C3b, lectins, antibodies...) enhance phagocytosis

3. Opsonisation

4.  Phagocytes are attracted to the site of infection by chemotactic substances (C5a, C3a and chemotactic products of bacteria)  absorbed bacteria are destroyed by the microbicidal systems (products of NADP-H oxidase, hydrolytic enzymes and bactericidal substances in lysosomes)  phagocytes produce proinflammatory cytokines (IL-1, IL-6, TNF) that induce an increase in temperature, metabolic response of the organism and synthesis of acute phase proteins

5. Phagocytosis

6.  in later stages of infection are stimulated antigen-specific mechanisms  plasma cells initially produce IgM isotype after isotype switching produce IgG1 and IgA (opsonization)  sIgA protect against intestinal and respiratory infections by bacteria  bacteria with a polysaccharide capsule may cause T-independent IgM antibody production (after the establishment to the bacteria activate the classical complement path)

7.  after infection persist IgG, IgA (protective effect) and memory T and B lymphocytes  in the defense against bacterial toxins apply neutralizing antibodies (Clostridium tetani and botulinum...)  "indirect toxins - bacterial Lipopolysaccharide (LPS) stimulates big number of monocytes to release TNF, which can cause septic shock  extracellular bacterial infections are especially at risk individuals with disorders in the function of phagocytes, complement and antibody production

9. Defense against intracellular pathogens

10.  bacteria, fungi and unicellular parasites  intracellular parasites are resistant to the microbicidal mechanisms of phagocytes  macrophages, which absorbed them, produce IL-12 → T H 1 differentiation, production of IFN  and membrane TNF → activation of macrophages and induction of iNOS

11. Defense against intracellular pathogens

12.  in the defense against intracelular parasites, which escape from phagolysosomes apply T C lymphocytes  intracellular microorganisms infections are at risk individuals with certain disorders of phagocytes and defects of T lymphocytes

13. Defense against intracellular pathogens

14. Anti-viral defense

15. Anti-viral defence  interferons - in infected cells is induced production of IFN  and IFN  (prevents viral replication and in uninfected cells cause the anti-virus status); IFN  stimulates the conversion to activated macrophages (iNOS)  IFN  and IFN  induce proliferation of  NK cells

16. Anti-viral defence - interferons

17.  NK cells - ADCC (Antibody-dependent cell-mediated cytotoxicity) = cytotoxic reaction depends on the antibodies; the NK-lymphocyte recognizes cell opsonized with IgG by stimulation Fc receptor CD16 and then activate cytotoxic mechanisms (degranulation)  infected macrophages produce IL-12 (a strong activator of NK cells)

18. NK cell activation

19.  in the defense against cytopathic viruses mostly applied antibodies:  sIgA inhibit mucosal adhesion of viruses (defense against respiratory viruses and enteroviruses)  neutralizing IgG and IgM antibodies activate the classical way of complement, which is capable of some viruses lysis  IgA and IgG derived in viral infection have a preventive effect in secondary infection

20. Anti-viral defence - antibodies

21.  effector T C lymphocytes destroy infected cells in direct contact (granzym/perforin; FasL) and by produced cytokines (lymfotoxin)  some viruses after infection integrate into the host genome, where persist for years (varicella zoster, EBV, papillomavirus)  by these infections are at risk individuals with T lymphocyte immunodeficiency and with combined immune disorders  increased susceptibility to herpes infections in individuals with dysfunction of NK cells

22. Anti-viral defence – NK cells and Tc lymphocytes

23. Defense against multicellular parasites

24.  IgE, mast cells, basophils and eosinophils  T H 2 stimulation under the influence of IL-4 (mast cells and other APC stimulated by parasite)  T H 2 stimulate B cells with BCR-specific parasite antigens  isotype switching under the influence of IL-4 to IgE  IgE bind to Fc  RI on mast cells and basophils („antigen- specific receptors“)

25.  establish of multivalent antigen (multicellular parasite) using the IgE to highafinity Fc receptor for IgE (Fc  RI) aggregation of several molecules Fc  RI  initiate mast cell degranulation (cytoplasmic granules mergers with the surface membrane and release hydrolytic enzymes, proteoglycans, biogenic amines (histamine, serotonin)  activation of arachidonic acid metabolism (leukotriene C4, prostaglandin PGD2) - amplification of inflammatory responses  cytokine production by mast cell (TNF, TGF , IL-4, 5,6...) Mast cell activation

26. Activation of mast cell

27.  Histamine causes vasodilation, increased vascular permeability, erythema, edema, itching, contraction of bronchial smooth muscle, increases intestinal peristalsis, increased mucus secretion of mucosal glands in the respiratory tract and GIT (helps eliminate the parasite)  in later stages are activated T H 1 and are produced antibodies of other classes  eosinophils fagocyte complexes of parasitic particles with IgE via their receptors for IgE  eosinophils use against parasites extracellular bactericidal substances released from granules (eosinophil cationic protein, protease)

28. Defense against multicellular parasites - eosinophils