PMID- 8642352
OWN - NLM
STAT- MEDLINE
DCOM- 19960718
LR  - 20190508
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 183
IP  - 5
DP  - 1996 May 1
TI  - RANTES and macrophage inflammatory protein 1 alpha selectively enhance 
      immunoglobulin (IgE) and IgG4 production by human B cells.
PG  - 2397-402
AB  - We studied the effects of various chemokines including neutrophil-activating 
      peptide 2 (NAP-2), beta-thromboglobulin (beta-TG), platelet factor 4 (PF-4), 
      melanoma growth stimulating activity (GRO), gamma interferon-induced protein 
      (IP-10), regulated on activation, normal T expressed and secreted (RANTES), 
      macrophage inflammatory protein 1 alpha (MIP-1 alpha), MIP-1 beta, and monocyte 
      chemotactic protein 1 (MCP-1) on Immunoglobulin (IgE) and IgG4 production by 
      human B cells. None of these chemokines with or without interleukin (IL-4), 
      anti-CD40 or -CD58 monoclonal antibody (mAb), induced IgE and IgG4 production by 
      B cells from nonatopic donors. However, RANTES and MIP-1 alpha selectively 
      enhanced IgE and IgG4 production induced by IL-4 plus anti-CD40 or -CD58 mAb 
      without affecting production of IgM, IgG1, IgG2, IgG3, IgA1, or IgA2, whereas 
      other chemokines failed to do so. Enhancement of IgE and IgG4 production by 
      RANTES and MIP-1 alpha was specifically blocked by anti-RANTES mAb and anti-MIP-1 
      alpha antibody (Ab), respectively, whereas anti-IL-5 mAb, anti-IL-6 mAb, 
      anti-IL-10 Ab, anti-IL-13 Ab, and anti-tumor necrosis factor-alpha mAb failed to 
      do so. Purified surface IgE positive (slgE4) and slgG4+ B cells generated either 
      in vitro or in vivo spontaneously produced IgE and IgG4, respectively, whereas 
      sIgE- and sIgG4- B cells failed to do so. RANTES and MIP-1 alpha enhanced 
      spontaneous IgE and IgG4 production in slgE+ and slgG4- B cells, respectively, 
      whereas neither RANTES nor MIP-1 alpha did so in sIgE- or sIgG4- B cells. 
      Purified sIgE4+ and sIgG4+, but not sIgE- or sIgG4- B cells, generated in vitro 
      and in vivo expressed receptors for RANTES and MIP-1 alpha, whereas they failed 
      to express receptors for other chemokines. These findings indicate that RANTES 
      and MIP-1 alpha enhance IgE and IgG4 production by directly stimulating sIgE+ and 
      sIgG4+ B cells.
FAU - Kimata, H
AU  - Kimata H
AD  - Department of Pediatrics, Yunichika Central Hospital, Kyoto, Japan.
FAU - Yoshida, A
AU  - Yoshida A
FAU - Ishioka, C
AU  - Ishioka C
FAU - Fujimoto, M
AU  - Fujimoto M
FAU - Lindley, I
AU  - Lindley I
FAU - Furusho, K
AU  - Furusho K
LA  - eng
PT  - Comparative Study
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 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Cytokines)
RN  - 0 (Growth Inhibitors)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Interferon Type I)
RN  - 0 (Interleukin-13)
RN  - 0 (Interleukin-2)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monokines)
RN  - 0 (Recombinant Proteins)
RN  - 130068-27-8 (Interleukin-10)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Antibody Formation/drug effects
MH  - B-Lymphocytes/drug effects/*immunology
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokine CCL5/*pharmacology
MH  - Cytokines/*pharmacology
MH  - Growth Inhibitors/pharmacology
MH  - Humans
MH  - Immunoglobulin E/*biosynthesis
MH  - Immunoglobulin G/*biosynthesis/classification
MH  - Interferon Type I/pharmacology
MH  - Interleukin-10/pharmacology
MH  - Interleukin-13/pharmacology
MH  - Interleukin-2/pharmacology
MH  - Interleukin-4/pharmacology
MH  - Kinetics
MH  - Macrophage Inflammatory Proteins
MH  - Monokines/*pharmacology
MH  - Palatine Tonsil/immunology
MH  - Recombinant Proteins/pharmacology
PMC - PMC2192590
EDAT- 1996/05/01 00:00
MHDA- 1996/05/01 00:01
PMCR- 1996/11/01
CRDT- 1996/05/01 00:00
PHST- 1996/05/01 00:00 [pubmed]
PHST- 1996/05/01 00:01 [medline]
PHST- 1996/05/01 00:00 [entrez]
PHST- 1996/11/01 00:00 [pmc-release]
AID - 96235052 [pii]
AID - 10.1084/jem.183.5.2397 [doi]
PST - ppublish
SO  - J Exp Med. 1996 May 1;183(5):2397-402. doi: 10.1084/jem.183.5.2397.