PMID- 7894201
OWN - NLM
STAT- MEDLINE
DCOM- 19950426
LR  - 20071115
IS  - 1018-8916 (Print)
IS  - 1018-8916 (Linking)
VI  - 13
IP  - 6
DP  - 1994 Nov-Dec
TI  - Increase in tumor necrosis factor-alpha mRNA but not perforin mRNA expression in 
      response to two newly characterized anti-LFA-1 monoclonal antibodies.
PG  - 301-14
AB  - We have generated two monoclonal antibodies (mAb), designated anti-1B11 and 
      anti-4F9, directed to the human lymphocyte-function-associated antigen-1 (LFA-1). 
      Indirect immunofluorescence with both mAb showed a bimodal distribution of 
      antigen on the surface of T, natural killer (NK), and lymphokine-activated killer 
      (LAK) cells. Neither mAb reacted with the epitopes recognized by TA1 and Mo-1 mAb 
      on the alpha-chain of the heterodimer. Anti-1B11 and anti-4F9 immunoprecipitated 
      polypeptide chains with molecular weights of 177 and 95 kD. Both mAb inhibited 
      cytolytic T lymphocytes (CTL), NK, and LAK cell-mediated cytotoxicity without 
      affecting antibody-dependent cellular cytotoxicity (ADCC). The proliferative 
      responses of T cells to allogeneic cells were inhibited by anti-1B11 and 
      anti-4F9, whereas the responses to phytohemagglutinin P and concanavalin A were 
      not affected. Anti-1B11 and anti-4F9 blocked effector cell (EC)-target cell (TC) 
      conjugate formation by 50%. Only anti-4F9 cross-reacted with LFA-1 on porcine 
      peripheral blood lymphocytes and inhibited porcine NK, LAK, and ADCC activities. 
      Because LFA-1 also functions at the level of signal transduction during T cell 
      activation and we previously showed that CTL rapidly degraded perforin and tumor 
      necrosis factor-alpha (TNF alpha) mRNA after interaction with sensitive TC, we 
      examined the effects of the mAb on the messages for perforin and TNF alpha. 
      Treatment of CTL with anti-1B11 and anti-4F9 induced TNF alpha message and 
      protein levels of TNF alpha, but did not alter perforin mRNA levels.
FAU - Hommel-Berrey, G
AU  - Hommel-Berrey G
AD  - Department of Medicine, Indiana University School of Medicine, Indianapolis 
      46202-5128.
FAU - Bochan, M
AU  - Bochan M
FAU - Brahmi, Z
AU  - Brahmi Z
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Nat Immun
JT  - Natural immunity
JID - 9206126
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Lymphocyte Function-Associated Antigen-1)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Pore Forming Cytotoxic Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126465-35-8 (Perforin)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/*immunology
MH  - Cell Line
MH  - Cytotoxicity Tests, Immunologic
MH  - Female
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Killer Cells, Lymphokine-Activated/immunology
MH  - Killer Cells, Natural/immunology
MH  - Lymphocyte Activation/immunology
MH  - Lymphocyte Function-Associated Antigen-1/*immunology
MH  - Lymphocyte Subsets/*immunology
MH  - Membrane Glycoproteins/*biosynthesis
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Perforin
MH  - Pore Forming Cytotoxic Proteins
MH  - Precipitin Tests
MH  - RNA, Messenger/*biosynthesis
MH  - Swine
MH  - T-Lymphocytes, Cytotoxic/immunology
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 1994/11/01 00:00
MHDA- 1994/11/01 00:01
CRDT- 1994/11/01 00:00
PHST- 1994/11/01 00:00 [pubmed]
PHST- 1994/11/01 00:01 [medline]
PHST- 1994/11/01 00:00 [entrez]
PST - ppublish
SO  - Nat Immun. 1994 Nov-Dec;13(6):301-14.