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M94B0781.TXT
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1994-11-11
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Document 0781
DOCN M94B0781
TI Interleukin-6 and the lung.
DT 9412
AU Zitnik RJ; Elias JA; Dept. of Internal Medicine, Yale Univ. Sch. of
Medicine, New; Haven, CT
SO Lung Biol Health Dis; 61:229-80 1993. Unique Identifier : AIDSLINE
ICDB/94606665
AB Interleukin-6 (IL6) is a pleiotropic cytokine produced by a wide variety
of cells, including many of the major cells in the lung, and in response
to a broad spectrum of stimuli (eg, viral infection, bacterial
endotoxin, agonists of cAMP, PKC, and calcium 2nd-messenger systems).
Regulation of IL6 production is complex and can occur at the level of
both gene transcription and mRNA degradation. The biological effects of
IL6 are protean, and newly discovered activities continue to be
described. IL6 production and activities are reviewed as follows: the
IL6 protein (structure, molecular heterogeneity, and structure-function
analysis), structure and regulation of the IL6 gene, the IL6 receptor,
biological effects of IL6 (B-cell and T-cell effects, plasmacytoma and
hybridoma growth, acute-phase response, hematopoiesis, and endocrine,
neurobiologic, and cutaneous effects), IL6 in human homeostasis (acute
inflammatory disorders, trauma and surgery, chronic inflammatory
disorders, neoplastic disorders, transplant rejection, and HIV and
Kaposi's sarcoma), and IL6 in the lung. IL6 causes disease by three
major mechanisms: (1) IL6 can be overproduced, causing disease as a
direct result of its systemic effects; (2) IL6 can be elevated as a
protective reaction to stress, injury, or infections; and (3) IL6 may
function as a part of dysregulated autocrine and paracrine feedback
loops in chronic inflammatory disease and neoplastic disorders. In the
pathogenesis of several neoplastic disorders, the effects of IL6 are
mediated principally through two major mechanisms: some tumors
constitutively produce large amounts of IL6, and the oversecreted
cytokine produces the systemic manifestations of the tumor; other tumors
constitutively produce and proliferate in response to IL6. The autocrine
or paracrine (or both) effects of IL6 on the tumor are responsible for
stimulating tumor cell proliferation and induction of the malignant
phenotype. Hematological malignancies (multiple myeloma, leukemias, and
lymphomas) and solid tumors are discussed. Several questions remain to
be answered concerning IL6 and its role in the lung. Particular
attention needs to be directed toward determining whether dysregulated
autocrine or paracrine IL6 feedback loops play an important role in the
pathogenesis of diseases such as sarcoidosis, asthma, hypersensitivity
pneumonitis, allograft rejection, and lung cancer. (247 Refs)
DE Cell Division Gene Expression Regulation Human
Interleukin-6/GENETICS/*METABOLISM Lung/*METABOLISM Lung
Diseases/METABOLISM Phenotype RNA, Messenger/METABOLISM
Transcription, Genetic MONOGRAPH
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).