Document 0904
 DOCN  M9650904
 TI    IL-4 producing CD4+ TCR alpha beta int liver lymphocytes: influence of
       thymus, beta 2-microglobulin and NK1.1 expression.
 DT    9605
 AU    Emoto M; Emoto Y; Kaufmann SH; Department of Immunology, University of
       Ulm, Germany.
 SO    Int Immunol. 1995 Nov;7(11):1729-39. Unique Identifier : AIDSLINE
       MED/96162431
 AB    The present report describes developmental, phenotypic and functional
       features of unconventional CD4+ TCR alpha beta lymphocytes. In C57BL/6
       mice, the majority of liver lymphocytes expressing intermediate
       intensity of TCR alpha beta (TCR alpha beta int) are CD4+ NK1.1+ and
       express a highly restricted TCR V beta repertoire, dominated by V beta 8
       with some contribution by V beta 7 and V beta 2. Although these cells
       express the CD4 co-receptor, they are present in H2-1 A beta (A beta)-/-
       gene disruption mutants but are markedly reduced in beta 2-microglobulin
       (beta 2m)-/- mutant mice and hence are beta 2m dependent. Thymocytes
       expressing the CD4+ NK1.1+ TCR alpha beta phenotype are also beta 2m
       contingent, suggesting that these two T lymphocyte populations are
       related. The CD4+ NK1.1+ TCR alpha beta lymphocytes in liver and thymus
       share several markers such as LFA-1+, CD44+, CD5+, LECAM-1- and IL-2R
       alpha-. The CD4+ NK1.1+ TCR alpha beta int liver lymphocytes were not
       detected in athymic nu/nu mice. We conclude that beta 2m expression is
       crucial for development of the CD4+ NK1.1+ TCR alpha beta int liver
       lymphocytes and that thymus plays a major role. CD4+ TCR alpha beta int
       liver lymphocytes were also identified in NK1.1- mouse strains, there
       lacking the NK1.1 marker. We assume that the NK1.1 molecule is a
       characteristic marker of the CD4+ TCR alpha beta int liver lymphocytes
       in NK1.1+ mouse strains, although its expression is not obligatory for
       their development. The liver lymphocytes from beta 2m+/-, but not from
       beta 2m-/-, mice are potent IL-4 producers in response to CD3 or TCR
       alpha beta engagement and the IL-4 production by liver lymphocytes was
       markedly reduced by treatment with anti-NK1.1 mAb. We conclude that the
       CD4+ NK1.1+ TCR alpha beta int liver lymphocytes are capable of
       producing IL-4 in response to TCR stimulation.
 DE    beta 2-Microglobulin/BIOSYNTHESIS/*PHYSIOLOGY  Animal
       Antigens/BIOSYNTHESIS/*PHYSIOLOGY  CD4 Lymphocyte Count  CD4-Positive
       T-Lymphocytes/CLASSIFICATION/*METABOLISM  Female  H-2
       Antigens/PHYSIOLOGY  Histocompatibility Antigens Class II/PHYSIOLOGY
       Immunophenotyping  Interleukin-4/*BIOSYNTHESIS  Killer Cells,
       Natural/*IMMUNOLOGY  Liver/CYTOLOGY/*IMMUNOLOGY  Male  Mice  Mice,
       Inbred Strains  Mice, Mutant Strains  Mice, Nude
       Proteins/BIOSYNTHESIS/*PHYSIOLOGY  Receptors, Antigen, T-Cell,
       alpha-beta/*BIOSYNTHESIS/GENETICS/  *IMMUNOLOGY  Support, Non-U.S. Gov't
       Thymus Gland/IMMUNOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).