Extracellular bacteria Disease is by two primary mechanisms:
Some bacteria are able to survive intracellular killing by phagocytic cells (e.g. Mycobacterium tuberculosis and Listeria monocytogenes).
1. IFN production by infected cells, and 2. direct killing of virus infected cells by natural killer (NK) cells. These mechanisms are especially important in the very early course of viral infections (before the immune response develops).
1. Specific Abs early in infection. Secretory immunity (IgA) is the basis for immunity to many viruses of the respiratory and GI tracts. This type of immunity is the target of oral vaccines. Humoral immunity also provides long-lasting protection after infections are cleared. Circulating immune complexes (Ag-Ab) may lodge in blood vessels and initiate C' mediated tissue damage.
2. Cytotoxic T lymphocytes (TC) are the principle mechanism for combating established viral infections. Tc directly kill virus infected host cells and may be responsible for tissue injury in non-cytopathic virus infections. Molecular mimicry may induce immune responses to self Ags.
Many of the larval stages (that develop in invertebrate hosts) activate C' and are susceptible to intracellular killing by phagocytes, whereas the parasitic forms that develop in human hosts are resistant.
Many protozoa have a pellicle, fungi have cell walls, and worms may have a thick protective tegument.
1. Specific IgE and eosinophilia are elicited by many helminths (blood flukes and Trypanosomes). Enhancement of inflammation is an important anti-parasitic strategy.
2. Cytokines from TH cells direct and modulate immune responses. A problem is that many parasites elicit inappropriate immune response. (Often an antibody response, which may not be very protective, is preferentially stimulated, instead of a T cell response which may be more protective).
3. CTL's that kill host cells infected with intracellular parasites or directly attack helminths.
4. Some parasites and/or their products induce granulomatous inflammation and fibrosis.
5. Polyclonal B cell activation may be stimulated by parasite surface products, but could result in immune complex disease or production of autoreactive Abs.