T lymphocytes, sensitized

These reactions are mediated by production of sensitized T-lymphocytes. On contact with antigen, an inflammatory reaction is generated which includes contact dermatitis, fever and photosensitization. 

Attempts continue to predict metal sensitivity in the individual patient so that the choice of material can be made accordingly. In vitro tests for metal allergies have been developed on the basis of lymphokine (MIF) release from sensitized T lymphocytes exposed to metal-protein complexes (11). About 6% of patients without a previous metal implant had positive reactions to nickel, chromium, or cobalt. However, it is still not clear whether such a positive reaction is a reliable predictor of clinical problems. In practice few patients have either local or systemic reactions when symptoms occur and other causes are ruled out, the implant should be removed. Some workers recommend removal of an implant whenever there is both a positive MIF test and a positive skin test, even in the current absence of a serious reaction. Allergic dermatitis will clear up as soon as the metal has begun to be cleared from the tissue. The type of metal and the amount released into the tissue will affect the time taken for the disappearance of toxic dermatological phenomena. 

The glomerular capillary wall is particularly susceptible to immune-mediated injury. Antigen and antibody tend to localize in the glomerulus, probably because of its high blood flow and capillary hydrostatic pressure. Parenchymal damage can be induced as a result of humoral- and cell-mediated immune reactions (Table 47-1). Antibodies and sensitized T lymphocytes are the primary mediators of glomerular injury. ... 

INABA, K. STEINMAN, R.M. (1984) Resting and sensitized T lymphocytes exhibit distinct (antigen presenting cell) requirements for growth and lymphokine release. Journal of Experimental Medicine, 160, 1717-1735. 

Thus, both specific circulating antibodies and sensitized T-lymphocytes are involved... 

Antibodies or sensitized T-lymphocytes reacting to the drug or to its metabolites may be demonstrated. 

Fig. 1. Schematic representation of the possible reactions of the immune system to drugs. A drug is probably presented as antigen most efficiently after binding to macrophage membranes and interacting with T-helper lymphocytes, which may either generate effector-sensitized T-lymphocytes or cooperate with B-l3miphocytes in the production of antidrug antibodies. This scheme of T/B cooperation is extremely oversimplified, since the various circuits of T-helper and suppressor cells are not represented (Germain et al. 1981)...

Interaction of antigenic determinants on target cells with sensitized T-lymphocytes leading to the activation of such lymphocytes and to the destruction of target cells, possibly through the formation of lymphotoxins and/or of toxic peroxides. 

Type IV reactions (cell-mediated or delayed hypersensitivity reactions) Type IV reactions are initiated when hapten-protein antigenic complex-mediated sensitized T lymphocytes meet the assaulting immunogen for the second time usually this leads to severe inflammation. Type IV reactions are exemplified by confact dermatitis. 

Type IV. Cellular mediated. Antigens, which are localized by direct contact with body tissue and bind to these tissues, react with im-mune-sensitized T-lymphocytes, releasing cell-free factors resulting in tissue damage. Some examples of this mechanism are al-leigic contact dermatitis and graft-versus-host transplantation rejection. 

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