Immune effectors antibody

Else, K.J. and Grencis, R.K. (1996) Antibody-independent effector mechanisms in resistance to the intestinal nematode parasite Trichuris muris. Infection and Immunity 64, 2950-2954. 

Scallon, BJ. et al., Chimericanti- TNF-a monoclonal antibody cA2 binds recombinant transmembrane TNF-a and activates immune effector functions, Cytokine, 7, 251,1995. 

Antibody consists of fragment ab (Fab) domain that binds to the antigen and fragment c (Fc) domain that recruits immune effector cells. Accordingly, receptors for the constant region (Fc) of antibodies provide critical links between the cellular and humoral parts of the immune system (6). 

By the time they have reached the lungs, schistosomula are innately resistant to immune effector mechanisms that are capable of killing schistosomula newly transformed from cer-cariae. In part, this is a reflection of the fact that growing schistosomula develop the ability to avoid activating complement and to evade recognition by antibodies (see below), and therefore are no longer susceptible to antibody or complement-mediated cellular cytotoxicity. However, studies in which these evasion mechanisms have been experimentally bypassed have revealed underlying resistance to immune effector molecules (Moser et al., 1980) the basis of this resistance is unknown. 

Scallon, B. J., Moore, M. A., Trinh, H., Knight, D. M., and Ghrayeb, J. (1995). Chimeric anti-TNFa monoclonal antibody cA2 binds recombinant transmembrane TNFa and activates immune effector functions. Cytokine1 , 251-259. 

ACAID Anterior chamber-associated immune deviation-a unique form of immune tolerance. ACAID is a selective, systemic immune deficiency where Antigen-specific delayed hypersensitivity and complement-fixing antibody responses are impaired by lymphocyte responses while other immune effectors are left preserved. 

IgA is the principal antibody present in a number of secretions and is the major antibody associated with the external immune system. IgA lacks the effector functions identified previously and acts mainly in immune exclusion (prevention of entry of potentially infectious entities into the body). As noted previously, there are differences in the immune effector mechanisms associated with the internal immune system or systemic immunity and the external immune system or local immunity. Systemic immunity is mediated by IgM and IgG, the latter is the major form of Ig found in the blood. Local immunity is mediated primarily by IgA and IgE. The contribution by the external immune system should not be underestimated because about half of the body s lymphocytes are associated with this system. 

In addition to those mentioned above, other chemicals have been implicated in the induction of occupational asthma. Some of these are listed in Table 1.1 and more comprehensive details are available elsewhere (Chan-Yeung and Malo, 1993). It is important to emphasize, however, that the inclusion of a chemical in such lists does not necessarily imply that respiratory symptoms result in all instances from allergic sensitization. For many chemicals associations have been found between respiratory effects and the presence of homocytotropic (IgE or IgG4) antibodies. Such associations are not universal and there is some uncertainty about the nature of immune effector mechanisms, and indeed the requirement for immune processes per se, in some forms of chemical-induced asthma. The subject of this book is allergic sensitization... 

The benchmark for the purification of most IgG species is Protein A, a 42 kDa molecular weight protein derived from a strain of Staphylococcus aureus. The natural molecule is located on the outer membrane surface of Staphylococcus aureus, and is linked to the cell surface through its C-terminal region [139]. This allows the pathogen to bind the Fc part of the IgG and re-direct the anti-gen-binding domain. This prevents interaction of the Fc part of the antibody with effector cells, thereby circumventing the activation of the immune system. 

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