Experiments On Inflammatory Cells
One must know how T-cells are attracted to sites of inflammation.
During the past decade scientific knowledge on the presence or absence of pro inflammatory versus regulatory subsets are known to have major effects on the course and outcome of inflammatory reactions, due primarily to distinct cytokines secreted. Intervention in these mechanisms may be of therapeutic value. Inflammation activates leucocytes locally which infiltrate diseased tissues.
Most organs lack significant lymphocyte movement in the non-inflamed state. The inflammatory process locally activates leucocytes which infiltrate diseased tissue. The mechanisms regulating adhesions are similar to those regulating the transmigration of lymphocytes.
Early investigations of lymphocyte trafficking indicate they may display organ-specific homing patterns. A variety of experimental and clinical studies have demonstrated that blocking either adhesion molecules or chemokines, chemical messengers could control autoimmune diseases such as rheumatoid arthritis or systemic lupus erythematosus. Leucocyte-endothelial cell interactions are mediated by cell adhesion molecules which facilitates trafficking in all animal species. Inhibiting leucocyte mediated tissue damage through non-specific inhibition of pro-inflammatory mediators using NSAIDs glucocorticoids and cytokines is quite successful. Through understanding leucocyte cell interactions, therapeutic strategies are being developed in several animal models and diseases, the clinical benefits gained will overcome damage caused by excessive leucocyte infiltration.
Animal studies clearly show how adhesion molecules and chemokine labelling can follow the transmigration of leucocytes. Rheumatology and Oncology studies on animals trace the damage done to inflamed tissues and organs, the resultant swelling disrupts organ or tissue function.
Transmigration of leucocytes causes damage to tissues and organs. Labelling of transmigrating leucocytes following the inflammatory response by means of monoclonal antibodies , radioactive isotopes and simply by tracing the end result provide an understanding of how leucocyte cell interactions can cause organ disruption. Animal studies allow therapeutic strategies for clinical benefits to overcome damage caused by excessive leucocyte infiltration.
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