NDLI: Selective inhibition of interleukin 2 gene function following thymocyte antigen/major histocompatibility complex receptor crosslinking: possible thymic selection mechanism. (Journal: Proceedings of the National Academy of Sciences of the United States of America Volume: 83 Issue: 18)

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Selective inhibition of interleukin 2 gene function following thymocyte antigen/major histocompatibility complex receptor crosslinking: possible thymic selection mechanism. (Journal: Proceedings of the National Academy of Sciences of the United States of America Volume: 83 Issue: 18)

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Selective inhibition of interleukin 2 gene function following thymocyte antigen/major histocompatibility complex receptor crosslinking: possible thymic selection mechanism. (Journal: Proceedings of the National Academy of Sciences of the United States of America Volume: 83 Issue: 18)

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ramarli, D. Milanese, C. Reinherz, E. L. Fox, D. A.
Abstract	Considerable evidence now exists to support the notion that the 50-kDa sheep erythrocyte-binding protein, T11, represents an essential cell surface component of a human T-cell lineage activation pathway. Furthermore, it is known that the human T3-Ti T-cell antigen/major histocompatibility complex receptor complex is capable of regulating cell growth mediated by the T11 structure. Here we show that, within the T3+ thymocyte compartment, T3-Ti crosslinking rapidly inhibits T11-initiated interleukin 2 (IL-2) gene transcription and translation. This inhibition is restricted to the IL-2 gene (IL2) as transcription of both the IL-2-receptor gene (IL2R) and the Ti beta-chain gene (TCRB) are not affected (human gene designations are in parentheses). Perhaps more importantly, T3-Ti-mediated IL-2 inhibition of this type is not operational in peripheral T lymphocytes. The results imply that the majority of T3+ thymocytes are functionally distinct from peripheral T lymphocytes despite their T3+ phenotype and must possess a unique endogenous regulatory component for suppressing IL-2 gene activity. Moreover, since IL-2 is likely rate-limiting for growth within the thymus, the findings provide one plausible mechanism for thymic selection--namely, T3-Ti crosslinking of thymocytes upon interaction with self-major histocompatibility complex inhibits clonal expansion of high-affinity autoreactive cells.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	18
Volume Number	83
Language	English
Publisher	National Academy of Sciences
Publisher Date	1986-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Surface Physiology Interleukin-2 Genetics Major Histocompatibility Complex Receptors, Antigen, T-Cell T-Lymphocytes Immunology Antigens, Differentiation, T-Lymphocyte Biosynthesis Lymphocyte Activation Tetradecanoylphorbol Acetate Pharmacology Transcription, Genetic Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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