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We report a case of gold pulmonary toxicity in a patient with adult-onset Still's disease with dyspnea on exertion and a normal chest radiograph. Withdrawal of gold therapy resulted in complete resolution of pulmonary toxicity in our patient without the need for additional steroid therapy.
To investigate the role of immunity-related medical conditions in the etiology of pancreatic cancer, we analyzed data from a population-based case-control study of pancreatic cancer conducted in Shanghai during 1992 and 1993. Information on prior histories of selected auto-immune diseases and allergic conditions was obtained from 108 incident pancreatic-cancer cases and 275 age- and gender-frequency matched controls by face-to-face interviews using a structured questionnaire. A prior history of auto-immune diseases was associated with a 2-fold elevated risk of pancreatic cancer (95% CI = 1.0-4.2), with an indication of a dose-response relation for the number of reported diseases. In contrast, a prior history of allergic condition was related to reduced risk (OR = 0.6, 95% CI = 0.4-1.1). With the possible exception of drug allergy, such an inverse association was seen for virtually all allergic conditions., although none of the OR was statistically significant. This study suggests that host immune function may be involved in the etiology of pancreatic cancer. Further investigations into the mechanism of these observed associations are warranted.
Delayed-type hypersensitivity (DTH) is a prototypic T lymphocyte-mediated response to antigenic challenge. In this study, mononuclear cells infiltrating the skin during cutaneous response to tuberculin in presensitized human subjects (responders) and nonimmune controls were identified using monoclonal antibodies by indirect immunofluorescence. In both responders and controls the infiltrate consisted mainly of T lymphocytes (T11+ and OKT3+) and monocytes (OKM1+, 63D3+, Mo2+) which initially accumulated in proximity to small blood vessels and later infiltrated the interstitial dermis and epidermis. More T lymphocytes reacted with OKT4 than with OKT8. 6 h after tuberculin the ratio of OKT4/OKT8 in tissue from responders exceeded that in blood, whereas in tissues studied at 15-48 h and in all control tissues those ratios in blood and tissue were similar. Evidence of T lymphocyte activation was sought using monoclonal antibodies anti-Tac, OKT9, and OKT10. In responders but not in controls the proportion of infiltrating cells reactive with these antibodies increased during the course of DTH. The presence of activated T lymphocytes in tissue was not associated with a comparable increase in peripheral blood cell populations identified by anti-Tac and OKT10. Studies using anti-B1, Leu-7, and anti-IgD/IgM revealed comparatively few reactive cells. Dual-labeling studies demonstrated that most Leu-7--reactive cells also bound T11 while fewer bound OKM1 or OKT8 and that cells reactive with OKIa1 and T11 constituted largely nonoverlapping populations. Specific patterns of reactivity were not observed when tissues were stained with anti-human C3, or poly C9-MA, a monoclonal antibody reactive with a neoantigen on polymerized C9 of the membrane attack complex of complement. The number of epidermal Langerhans cells identified by OKT6 was similar in responders and controls. Thus, the cutaneous response to tuberculin in sensitized individuals is characterized by early enrichment of the OKT4 subpopulation of T lymphocytes in tissue infiltrates and subsequent (15-48 h) evidence of T lymphocyte activation.
Among extremely mathematically and/or verbally precocious students (top 1 in 10,000 in such reasoning ability), the following three physiological characteristics were found at high frequencies: left- or mixed-handedness, asthma and other allergies, and myopia. The first two of these may reflect the effects of a common influence (testosterone) on the nervous and immune systems during fetal development. Moreover, our results suggest that such highly able students may exhibit bihemispheric representation of cognitive functions. These results may bear on the etiology of intellectual talent.
The pathogenesis of autoimmune vasculitis is poorly understood. Understanding the immunologic mechanisms governing this disease requires precise identification of the cells which comprise the lesion. In this report, we have evaluated tissue sections from MRL/lpr mice from 16 to 45 weeks of age, representing all stages of clinical vasculitis. We demonstrate that basophil myelocytes participate in the evolution of the delayed-type hypersensitivity (DTH) response which initiates and perpetuates autoimmune vasculitis in these mice. These findings raise questions regarding the immunologic mechanisms by which basophils develop in this lesion and the interaction of basophils. VSMCs and lymphocytes in vasculitic angiodestruction.