PMID- 8086129
OWN - NLM
STAT- MEDLINE
DCOM- 19941020
LR  - 20190718
IS  - 0269-9370 (Print)
IS  - 0269-9370 (Linking)
VI  - 8
IP  - 6
DP  - 1994 Jun
TI  - Nef protein of HIV-1 has B-cell stimulatory activity.
PG  - 733-4
AB  - OBJECTIVE: To examine the B-cell stimulatory properties of the regulatory Nef 
      protein of HIV-1. METHODS: The effect of the HIV-1 regulatory proteins Nef, Tat 
      and Vif, were analyzed for their ability to induce differentiation of normal B 
      lymphocytes into immunoglobulin secreting cells (ISC). RESULTS: A recombinant Nef 
      protein, but neither Tat or Vif, was able to induce ISC in peripheral blood 
      lymphocyte (PBL) cultures of HIV-1-seronegative donors. Another recombinant Nef 
      protein, d-Nef, with a truncated amino terminal (deletion of 34 amino acids) 
      failed to induce B-cell differentiation. Pretreatment of the Nef protein with a 
      polyclonal anti-Nef-antibody abrogated its B-cell stimulatory activity. The 
      Nef-induced B-cell differentiation was dependent on cell-to-cell contact. Cell 
      surface molecules leukocyte function-associated molecule (LFA)-1, intracellular 
      adhesion molecule (ICAM)-1, human lymphocyte antigen-DR and B7 were involved in 
      the T-B-cell interaction because monoclonal antibodies to these molecules 
      abrogated the Nef-induced B-cell differentiation response. The Nef protein was 
      able to induce interleukin (IL)-6 messenger (m)RNA and IL-6 protein secretion in 
      PBL, with monocytes as the primary source. CONCLUSIONS: These findings indicate 
      that regulatory (Nef) proteins of HIV-1 contribute to the intense B-cell 
      activation that occurs in association with HIV-1 infection. T-B-cell 
      contact-dependent interaction and induction of IL-6 by these proteins appear to 
      play major roles in this process.
FAU - Chirmule, N
AU  - Chirmule N
AD  - Department of Pediatrics, North Shore University Hospital-Cornell University 
      Medical College, Manhasset, New York 11030.
FAU - Oyaizu, N
AU  - Oyaizu N
FAU - Saxinger, C
AU  - Saxinger C
FAU - Pahwa, S
AU  - Pahwa S
LA  - eng
GR  - AI28281/AI/NIAID NIH HHS/United States
GR  - RR05924-06/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (Gene Products, nef)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
RN  - 0 (nef Gene Products, Human Immunodeficiency Virus)
SB  - IM
MH  - B-Lymphocytes/*immunology
MH  - Cell Differentiation
MH  - Cells, Cultured
MH  - Gene Products, nef/*immunology
MH  - HIV-1/*immunology
MH  - Humans
MH  - Interleukin-6/genetics/metabolism
MH  - Lymphocyte Cooperation
MH  - Macrophages/cytology/immunology
MH  - Monocytes/cytology/immunology
MH  - RNA, Messenger/biosynthesis
MH  - Recombinant Proteins/metabolism
MH  - T-Lymphocytes/cytology/immunology
MH  - nef Gene Products, Human Immunodeficiency Virus
EDAT- 1994/06/01 00:00
MHDA- 1994/06/01 00:01
CRDT- 1994/06/01 00:00
PHST- 1994/06/01 00:00 [pubmed]
PHST- 1994/06/01 00:01 [medline]
PHST- 1994/06/01 00:00 [entrez]
AID - 10.1097/00002030-199406000-00002 [doi]
PST - ppublish
SO  - AIDS. 1994 Jun;8(6):733-4. doi: 10.1097/00002030-199406000-00002.