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The effects of cytokines and adherent cells on the interleukin 4-mediated induction of Ia antigens on resting B cells
Authors:K Oliver  P H Krammer  P W Tucker  E S Vitetta
Affiliation:1. Immunology Graduate Program, University of Texas Health Science Center, Southwestern Medical School, Dallas, Texas 75235 USA;2. Department of Microbiology, University of Texas Health Science Center, Southwestern Medical School, Dallas, Texas 75235 USA;3. The Institute for Immunology and Genetics, Heidelberg, Federal Republic of Germany;1. Division of Clinical Physiology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan;2. Department of Dental Anesthesiology, Kanagawa Dental University, Kanagawa, Japan;3. Department of Dental Anesthesiology, Okayama University, Okayama, Japan;4. Division of Dental Anesthesiology, Department of Science of Physical Functions, Kyushu Dental University, Fukuoka, Japan;5. Department of Dental Anesthesiology, Tokyo Medical and Dental University, Tokyo, Japan;6. Clinical Research Center, Nagasaki University Hospital, Nagasaki, Japan;7. Fisher & Paykel Healthcare Ltd, Auckland, New Zealand;1. Japan Dental Association Research Institute, Tokyo, Japan;2. Department of Dental Sociology, Kanagawa Dental University, Yokosuka, Japan;3. Japan Dental Association, Tokyo, Japan
Abstract:In this report we have extended our previous studies on interleukin 4 (IL-4) [previously termed B-cell stimulatory factor-1 (BSF-1)]. Our results demonstrate that 8 hr of exposure to IL-4 is sufficient to induce maximal expression of Ia antigens. This increase in expression of Ia antigens on resting B cells is due to the direct action of IL-4 on the B cells since adding or removing adherent cells or utilizing low density cultures of B cells at 50-100/culture had no effect on the IL-4-mediated increase in Ia. Monoclonal anti-IL-4 antibody completely abrogated the Ia-inducing activity of IL-4. A variety of other purified lymphokines including interleukin 2 (IL-2), interleukin 1 (IL-1), and a source of either B-cell differentiation factor for IgM (BCDF mu), or B-cell growth factor II (BCGF II), did not alter the expression of Ia antigens on resting B cells. However, interferon-gamma can partially inhibit the IL-4-mediated induction of Ia.
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