PMID- 8046348
OWN - NLM
STAT- MEDLINE
DCOM- 19940830
LR  - 20190508
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 180
IP  - 2
DP  - 1994 Aug 1
TI  - Growth hormone and insulin-like growth factor I induce immunoglobulin (Ig)E and 
      IgG4 production by human B cells.
PG  - 727-32
AB  - We studied the effects of growth hormone (GH), insulin-like growth factor I 
      (IGF-I), IGF-II, and insulin on human immunoglobulin E (IgE) and IgG4 production. 
      GH and IGF-I induced IgE and IgG4 production by normal donors' mononuclear cells 
      (MNC) depleted of sIgE+ and sIgG4+ B cells without affecting IgM, IgG1, IgG2, 
      IgG3, IgA1, or IgA2 production, whereas IGF-II and insulin failed to do so. 
      GH-induced IgE and IgG4 production was specific, and was not mediated by IGF-I, 
      interleukin 4 (IL-4), or IL-13, since it was blocked by anti-GH antibody (Ab), 
      but not by anti-IGF-I Ab, anti-IL-4 Ab, or anti-IL-13 Ab. Conversely, 
      IGF-I-induced IgE and IgG4 production was blocked by anti-IGF-I Ab, but not by 
      anti-GH Ab, anti-IL-4 Ab, or anti-IL-13 Ab. Moreover, interferon alpha 
      (IFN-alpha) or IFN-gamma, which counteracted IL-4-and IL-13-induced IgE and IgG4 
      production, had no effect on induction by GH or IGF-I. In contrast to MNC, GH or 
      IGF-I failed to induce IgE and IgG4 production by purified sIgE-, sIgG4- B cells. 
      However, in the presence of anti-CD40 monoclonal antibody (mAb), GH or IGF-I 
      induced IgE and IgG4 production by these cells. Purified sIgE+, but not sIgE-, B 
      cells from atopic patients spontaneously produced IgE. GH or IGF-I with anti-CD40 
      mAb failed to enhance IgE production by sIgE+ B cells, whereas they induced IgE 
      production by sIgE- B cells. Similarly, whereas GH or IGF-I with anti-CD40 mAb 
      failed to enhance IgG4 production by sIgG4+ B cells from atopic patients, they 
      induced IgG4 production by sIgG4- B cells. Again, neither IgE nor IgG4 induction 
      was blocked by anti-IL-4 Ab or anti-IL-13 Ab. These results indicate that GH and 
      IGF-I induce IgE and IgG4 production by class switching in an IL-4- and 
      IL-13-independent mechanism.
FAU - Kimata, H
AU  - Kimata H
AD  - Department of Pediatrics, Kyoto University Hospital, Japan.
FAU - Fujimoto, M
AU  - Fujimoto M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (Immunoglobulin G)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 9002-72-6 (Growth Hormone)
SB  - IM
MH  - B-Lymphocytes/*immunology
MH  - Cells, Cultured
MH  - Growth Hormone/*physiology
MH  - Humans
MH  - Immunoglobulin E/*biosynthesis/immunology
MH  - Immunoglobulin G/*biosynthesis/immunology
MH  - Insulin-Like Growth Factor I/*physiology
MH  - Monocytes/immunology
PMC - PMC2191604
EDAT- 1994/08/01 00:00
MHDA- 1994/08/01 00:01
PMCR- 1995/02/01
CRDT- 1994/08/01 00:00
PHST- 1994/08/01 00:00 [pubmed]
PHST- 1994/08/01 00:01 [medline]
PHST- 1994/08/01 00:00 [entrez]
PHST- 1995/02/01 00:00 [pmc-release]
AID - 94321931 [pii]
AID - 10.1084/jem.180.2.727 [doi]
PST - ppublish
SO  - J Exp Med. 1994 Aug 1;180(2):727-32. doi: 10.1084/jem.180.2.727.