PMID- 1511960
OWN - NLM
STAT- MEDLINE
DCOM- 19920929
LR  - 20131121
IS  - 0367-6102 (Print)
IS  - 0367-6102 (Linking)
VI  - 67
IP  - 3
DP  - 1992 May
TI  - Functional and phenotypic analyses of thymic low density adherent cells from 
      murine bone marrow chimeras--influence on thymocyte differentiation.
PG  - 376-97
AB  - Previous studies from this laboratory demonstrated a malfunction of the thymus of 
      C3H mice to induce normal level of thymocyte differentiation. Thymocytes 
      developed in the C3H thymus showed depressed proliferative responses to 
      stimulation with anti-CD3 antibody compared with those developed in the other 
      strains. This study was conducted to analyze immunological functions of the 
      thymic stromal cell population in the C3H mice. Using allogeneic bone marrow (BM) 
      chimeras established by reciprocal combination of AKR and C3H mice as donor or 
      recipient, antigen presenting cell (APC) function of low density adherent cells 
      (LDAC) in the thymus was analyzed. The thymic LDAC from C3H mice or [AKR----C3H] 
      BM chimeras where AKR were BM donors and C3H were recipients contained high 
      proportion of Mac-1+ cells as compared to AKR mice or [C3H----AKR] chimeras. The 
      proportion of Mac-1+ cells paralleled the IL-1 secreting ability of the LDAC. 
      Thus, the higher proportion of Mac-1+ cell in the thymus may be responsible for 
      low accessory function observed in C3H thymuses. However, when APC function was 
      analyzed using various T cell hybridomas or a T cell line, the APC functions did 
      not necessarily correlate to the proportions of Mac-1+ cells and amounts of IL-1 
      produced by the LDAC. When proliferative responses of thymocytes to anti-CD3 
      stimulation were analyzed in the presence of prostaglandins, PGE-2 inhibited more 
      profoundly the responses of [AKR----C3H] and normal C3H mice than those of 
      [C3H----AKR] and normal AKR mice. Furthermore, a prostaglandin inhibitor, 
      indomethacin, reversed the depressed responses of the former thymocytes which had 
      developed in the C3H thymus. These findings suggest that the hyporesponsiveness 
      of thymocytes from [AKR----C3H] chimeras to anti-CD3 stimulation may be 
      attributable to their increased sensitivity to prostaglandin produced by LDAC.
FAU - Wambua, P P
AU  - Wambua PP
AD  - Institute of Immunological Science, Hokkaido University, Sapporo, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Hokkaido Igaku Zasshi
JT  - [Hokkaido igaku zasshi] The Hokkaido journal of medical science
JID - 17410290R
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Surface)
RN  - 0 (Interleukin-1)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Antigen-Presenting Cells/immunology/metabolism
MH  - Antigens, CD/immunology
MH  - Antigens, Surface/analysis
MH  - Bone Marrow Transplantation/*immunology
MH  - *Cell Differentiation
MH  - Chimera/*immunology
MH  - Dinoprostone/pharmacology
MH  - Interleukin-1/metabolism
MH  - Lymphocyte Subsets/*immunology
MH  - Mice
MH  - Thymus Gland/*cytology/immunology
EDAT- 1992/05/01 00:00
MHDA- 1992/05/01 00:01
CRDT- 1992/05/01 00:00
PHST- 1992/05/01 00:00 [pubmed]
PHST- 1992/05/01 00:01 [medline]
PHST- 1992/05/01 00:00 [entrez]
PST - ppublish
SO  - Hokkaido Igaku Zasshi. 1992 May;67(3):376-97.