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Fourteen monoclonal antibodies were used to immunohistochemically label 22 temporal artery biopsy specimens taken from patients with temporal arteritis before treatment (n = 10), after 1.3 days of corticotherapy (n = 6) and after 12-30 days of steroids (n = 6). Histological sections from untreated patients revealed an inflammatory infiltrate comprised of approximately equal proportions of macrophages and T lymphocytes; the majority of the latter belonged to the CD4+ subset (the CD4+/CD8+ ratio varied from 2/1 to 4/1, depending upon the biopsy). These cells expressed high levels of HLA DR and low levels of interleukin-2 (IL2) receptors. A few B lymphocytes and plasmocytes were seen, mainly in the adventitia. Antigen-presenting cells (APC) were always found in the damaged media and natural killer cells (few in number) were sometimes present. Some macrophages were positively immunolabeled for IL6. A short, 1-to-3-day course of corticosteroids did not appreciably modify the lesions: cells remained highly activated, APC were seen in half the biopsies and IL6 immunolabeling persisted. The findings were essentially the same in treated but poorly controlled patients. Biopsies from 2 patients in clinical and biological remission revealed the persistence of an active immunological process. These observations indicate that the immunological process is poorly controlled by corticosteroid therapy.

We used in situ hybridization to study the expression of interleukin genes in sarcoidosis and in persistent generalized lymphadenopathy of HIV disease. In both cases, we found a dramatic over-expression of the interferon-gamma (IFN gamma) gene as compared to that of the interleukin-2 (IL-2) gene. In sarcoidosis, IFN gamma producing cells are CD4 T cells and are associated with IL-1 beta gene expressing monocytic cells. In HIV lymphadenopathy IFN gamma producing cells are C8 T cells engaged in cytotoxic function, as evidenced by the concomitant expression of serine esterase B gene. Thus distinct patterns of interleukin production can be defined in vivo in selected immunopathological situations.

New methods allow the study of humoral immunity in man using blood lymphocyte cultures. A primary in vitro antibody response can be induced, characterized by the appearance of antibody forming cells, and its pattern is as follows: stringent culture requirements, which have been so far obtained in few laboratories; the kinetics of the response, with a peak on day 7--8; and exclusively IgM response; a T-cell requirement. Among these methods, the model we have described has the advantage of allowing a reproductible response in a given individual. The in vitro study of humoral immunity has limitations, the most apparent of which is that it addresses itself to only one lymphoid population, that in peripheral blood, easily accessible. It presents several advantages, as compared to an in vivo study after injection of an antigen: absence of ethical problem; the necessity of only one blood sample, at a given time, avoiding the interference of a treatment started after the test; the possibility of performing successive primary stimulations for a longitudinal study.