PMID- 8070849
OWN - NLM
STAT- MEDLINE
DCOM- 19940929
LR  - 20191023
IS  - 0882-0139 (Print)
IS  - 0882-0139 (Linking)
VI  - 23
IP  - 3
DP  - 1994 Apr
TI  - IL-6 mediated isotype specific suppression of hapten specific IgE in serum of 
      BPO-KLH sensitized mice: role of IFN alpha in maintainance of hapten specific IgE 
      responses.
PG  - 213-21
AB  - The ability of IL-6 or IFN alpha or antibodies to these cytokines to regulate 
      serum levels of hapten specific immunoglobulins (IgM, IgG1, IgE, IgA) was studied 
      in BPO-KLH (benzylpenicilloyl-keyhole limpet hemocyanin) sensitized BALB/c mice 
      at the peak of a hapten specific IgE antibody forming cell (AFC) response. To 
      induce peak IgE responses, mice were injected intraperitonealy (i.p.) with 
      BPO-KLH (10 micrograms) in aluminum hydroxide gel (alum) on days 0, 21, and 42. 
      On day 44, mice were injected s.c. with IL-6 (100-1000 U), IFN alpha (1000-10,000 
      U), anti-IL-6 (100-1000 neutralizing units [NU]), or anti-IFN alpha (1000-10,000 
      NU). On day 46, levels of BPO specific IgM, IgG1, IgE and IgA in serum were 
      determined (ELISA). Data are expressed as micrograms/ml. IL-6 suppressed BPO 
      specific IgE in serum in isotype specific fashion (to > 90%), increasing IgA 
      (approximately 3 fold), and leaving IgM and IgG1 unchanged. Since removal of 
      endogenous IL-6 with anti-IL-6 increased serum IgE, and suppressed IgG1 
      (approximately 50%), with IgM and IgA unchanged, this suggests that IL-6 is an 
      isotype specific suppressor of peak IgE responses and as such may be useful in 
      the therapeutic management of atopic disease. IFN alpha treatment increased serum 
      IgE levels (60%), and potentiated IgA responses (> 30 fold), with IgM and IgG1 
      unchanged. Since removal of endogenous IFN alpha with anti-IFN alpha decreased 
      IgE levels (approximately 50%), increasing IgA, with IgM and IgG1 unchanged, this 
      suggests a role for IFN alpha as an isotype specific helper of peak IgE responses 
      and in maintenance of IgA responses.
FAU - Auci, D L
AU  - Auci DL
AD  - Department of Pathology, State University of New York Health Science Center at 
      Brooklyn 11203.
FAU - Miller, H
AU  - Miller H
FAU - Chice, S M
AU  - Chice SM
FAU - Durkin, H G
AU  - Durkin HG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunol Invest
JT  - Immunological investigations
JID - 8504629
RN  - 0 (Benzeneacetamides)
RN  - 0 (Haptens)
RN  - 0 (Immunoglobulin Isotypes)
RN  - 0 (Interferon-alpha)
RN  - 0 (Interleukin-6)
RN  - 2642-55-9 (benzylpenicilloyl G)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 9013-72-3 (Hemocyanins)
RN  - FV4Y0JO2CX (keyhole-limpet hemocyanin)
RN  - Q42T66VG0C (Penicillin G)
SB  - IM
MH  - Animals
MH  - Antibody-Producing Cells/immunology
MH  - Benzeneacetamides
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Haptens
MH  - Hemocyanins/immunology
MH  - Immune Tolerance
MH  - Immunoglobulin E/*immunology
MH  - Immunoglobulin Isotypes/*immunology
MH  - Interferon-alpha/*immunology
MH  - Interleukin-6/*immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Penicillin G/analogs & derivatives/immunology
EDAT- 1994/04/01 00:00
MHDA- 1994/04/01 00:01
CRDT- 1994/04/01 00:00
PHST- 1994/04/01 00:00 [pubmed]
PHST- 1994/04/01 00:01 [medline]
PHST- 1994/04/01 00:00 [entrez]
AID - 10.3109/08820139409087801 [doi]
PST - ppublish
SO  - Immunol Invest. 1994 Apr;23(3):213-21. doi: 10.3109/08820139409087801.