HIV-1 GP41 BINDING-PROTEINS AND ANTIBODIES TO GP41 COULD INHIBIT ENHANCEMENT OF HUMAN RAJI CELL MHC CLASS-I AND CLASS-II EXPRESSION BY GP41

被引:20
作者
CHEN, YH
BOCK, G
VORNHAGEN, R
STEINDL, F
KATINGER, H
DIERICH, MP
机构
[1] INST HYG, A-6010 INNSBRUCK, AUSTRIA
[2] LUDWIG BOLTZMANN INST AIDS RES, INNSBRUCK, AUSTRIA
[3] INST GEN & EXPTL PATHOL, INNSBRUCK, AUSTRIA
[4] INST APPL MICROBIOL, VIENNA, AUSTRIA
[5] BIOTEST, DREIEICH, GERMANY
关键词
HIV-1; GP41; GP41-BINDING PROTEINS; ANTI-GP41; MABS; MHC EXPRESSION ENHANCEMENT;
D O I
10.1016/0161-5890(94)90092-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Based on our findings, that HIV-1 soluble gp41 could bind to several proteins on the human, T, B and monocyte cells independently of CD4, we examined the effect of HIV-1 soluble gp41 (sgp41; Env amino acids 539-684) on surface expression of MHC I and II, ICAM-1 and CD21 molecules on human Raji cells. Flow cytometry (FACS) analysis demonstrated that sgp41 could selectively enhance MHC class I and II expression on Raji cells, but did not increase expression of other cell surface antigens, such as, CD21 and CD54 (ICAM-1). Soluble gp41 could also enhance MHC class I and II expression on another human B cell line, Bjab. The sgp41-dependent enhancement of the MHC class I and II expression on Raji cells is time- and dose-dependent. The sgp41 enhancement effect on the MHC antigen expression could be inhibited by the gp41-binding proteins of 45, 49 and 62 kD (isolated from Raji-lysate) which could inhibit the sgp41-binding to Raji cells. Interestingly, this sgp41-dependent enhancement of the MHC class I and II expression could also be inhibited by two mAbs to HIV-1 gp41, but not by a third mAb binding to a different site on gp41. These results demonstrate that HIV-I sgp41 can selectively enhance the human Raji cell MHC class I and II antigen expression and this enhancement effect could be inhibited by the sgp41-binding proteins and anti-gp41 antibodies, and suggest that the sgp41-dependent enhancement is mediated by its binding to Raji membrane proteins of 45, 49 and 62 kD.
引用
收藏
页码:977 / 982
页数:6
相关论文
共 27 条
[1]   ISOLATION OF A T-LYMPHOTROPIC RETROVIRUS FROM A PATIENT AT RISK FOR ACQUIRED IMMUNE-DEFICIENCY SYNDROME (AIDS) [J].
BARRESINOUSSI, F ;
CHERMANN, JC ;
REY, F ;
NUGEYRE, MT ;
CHAMARET, S ;
GRUEST, J ;
DAUGUET, C ;
AXLERBLIN, C ;
VEZINETBRUN, F ;
ROUZIOUX, C ;
ROZENBAUM, W ;
MONTAGNIER, L .
SCIENCE, 1983, 220 (4599) :868-871
[2]   INTERNALIZATION OF THE HUMAN IMMUNODEFICIENCY VIRUS DOES NOT REQUIRE THE CYTOPLASMIC DOMAIN OF CD4 [J].
BEDINGER, P ;
MORIARTY, A ;
VONBORSTEL, RC ;
DONOVAN, NJ ;
STEIMER, KS ;
LITTMAN, DR .
NATURE, 1988, 334 (6178) :162-165
[3]   THE HUMAN MONOCYTE CELL-LINE U937 BINDS HIV-1 GP41 BY PROTEINS OF 37, 45, 49, 62 AND 92-KDA [J].
CHEN, YH ;
BOCK, G ;
VORNHAGEN, R ;
STEINDL, F ;
KATINGER, H ;
DIERICH, MP .
IMMUNOLOGY LETTERS, 1993, 37 (01) :41-45
[4]   HIV-1 GP41 BINDING TO HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS OCCURS PREFERENTIALLY TO B-LYMPHOCYTES AND MONOCYTES [J].
CHEN, YH ;
BOCK, G ;
VORNHAGEN, R ;
STEINDL, F ;
KATINGER, H ;
DIERICH, MP .
IMMUNOBIOLOGY, 1993, 188 (4-5) :323-329
[5]   HIV-1 GP41 CONTAINS 2 SITES FOR INTERACTION WITH SEVERAL PROTEINS ON THE HELPER T-LYMPHOID CELL-LINE, H9 [J].
CHEN, YH ;
EBENBICHLER, C ;
VORNHAGEN, R ;
SCHULZ, TF ;
STEINDL, F ;
BOCK, G ;
KATINGER, H ;
DIERICH, MP .
AIDS, 1992, 6 (06) :533-539
[6]   ENHANCEMENT OF HIV-1 GP41 BINDING TO RAJI CELLS BY PWM, LPS, INTERFERON-GAMMA AND INTERLEUKIN-6 [J].
CHEN, YH ;
OPITZ, S ;
BOCK, G ;
STEINDL, F ;
KATINGER, H ;
DIERICH, MP .
MOLECULAR IMMUNOLOGY, 1993, 30 (17) :1583-1586
[7]   DETECTION OF A FUSION PEPTIDE SEQUENCE IN THE TRANSMEMBRANE PROTEIN OF HUMAN-IMMUNODEFICIENCY-VIRUS [J].
GALLAHER, WR .
CELL, 1987, 50 (03) :327-328
[8]   FREQUENT DETECTION AND ISOLATION OF CYTOPATHIC RETROVIRUSES (HTLV-III) FROM PATIENTS WITH AIDS AND AT RISK FOR AIDS [J].
GALLO, RC ;
SALAHUDDIN, SZ ;
POPOVIC, M ;
SHEARER, GM ;
KAPLAN, M ;
HAYNES, BF ;
PALKER, TJ ;
REDFIELD, R ;
OLESKE, J ;
SAFAI, B ;
WHITE, G ;
FOSTER, P ;
MARKHAM, PD .
SCIENCE, 1984, 224 (4648) :500-503
[9]  
HALLORAN PF, 1986, TRANSPLANTATION, V41, P413, DOI 10.1097/00007890-198604000-00001
[10]  
HENDERSON LA, 1993, J BIOL CHEM, V268, P15291