Lymphocyte function-associated antigens one (LFA-1) on B and on T lymphocytes bind a monoclonal antibody with different affinities

Agthoven, AndréJ. van; Truneh, Alemseged

doi:10.1016/0008-8749(85)90048-6

Cited by 10 publications

(8 citation statements)

References 21 publications

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“…However, the antigen-induced T lymphocyte proliferation was found normal in the patient. Although expressed on the membrane of B lymphocytes, LFA-1 has been considered not to play a role at the B cell level (34). The present observation suggests that LFA-1 could be involved in T lymphocyte-B lymphocyte and/or MN-B lymphocyte interaction required for some antibody responses.…”

Section: Resultsmentioning

confidence: 58%

Deficiency of the adhesive protein complex lymphocyte function antigen 1, complement receptor type 3, glycoprotein p150,95 in a girl with recurrent bacterial infections. Effects on phagocytic cells and lymphocyte functions.

Fischer¹,

Seger²,

Durandy³

et al. 1985

J. Clin. Invest.

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A patient presenting delayed umbilical cord detachment, severe recurrent bacterial infections, and inability to form pus exhibited a profound defect in the expression of a-and 8-chains of the receptor for the C3bi fragment of C3 (CR3), lymphocyte function antigen I (LFA-1) molecule, and the p150,95 molecule found on neutrophils, monocytes, and lymphocyte membranes. This was shown by immunofluorescence studies using specific monoclonal antibodies, rosette formation with C3bi-coated erythrocytes, and immunoprecipitation for the LFA-1 complex. These membrane defects were responsible for abnormal phagocytic cell functions including adherence to nylon wool, cell movement, phagocytosis, and opsonized particle-induced oxidative response and for defective natural killer cell activity. In addition, lymphocyte function deficiencies previously unobserved in this disease were found. Cytolytic T lymphocyte activity was profoundly reduced; a-and y-interferon production were impaired. Finally, there was no antibody production to vaccinal antigens whereas the antibody responses to polysaccharides and to cytomegalovirus were found to be normal. The cytotoxic T cell deficiency could be expected from previous blocking experiments of this function with monoclonal antibodies to LFA-1 and is probably related to an extremely severe deficiency in LFA-1 expression in this patient. Anomalies in interferon and in antibody production suggest additional role(s) of the LFA-1 complex in monocyte/T lymphocyte/B lymphocyte cell interactions that have not yet been envisaged.

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Section: Resultsmentioning

confidence: 58%

Deficiency of the adhesive protein complex lymphocyte function antigen 1, complement receptor type 3, glycoprotein p150,95 in a girl with recurrent bacterial infections. Effects on phagocytic cells and lymphocyte functions.

Fischer¹,

Seger²,

Durandy³

et al. 1985

J. Clin. Invest.

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“…Since an anti-ICAM-1 mAb did not block conjugate formation between activated LFA-1-T and B lymphocytes while it partially blocked conjugate formation between LFA-1' T and B lymphocytes, one may conclude that ICAM-1 is a ligand for LFA-1 [12] [36].…”

Section: Discussionmentioning

confidence: 93%

The role of lymphocyte function‐associated antigen 1 (LFA‐1) in the adherence of T lymphocytes to B lymphocytes

et al. 1988

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The functional role of the LFA-1 molecule in the interaction between helper T lymphocytes and B lymphocytes was investigated using lymphocytes from patients with leukocyte adhesion deficiency, an inherited immunodeficiency characterized by a defective leukocyte expression of the LFA-1, Mac-1 (CR3) and p150,95 molecules. The ability of LFA-1- T lymphocytes to provide antigen-specific help for HLA-identical LFA-1+ B lymphocytes was reduced while their antigen-specific activation was normal. Antigen-independent conjugate formation between resting, nonactivated LFA-1- T lymphocytes and LFA-1+ B lymphocytes was impaired while LFA-1- B lymphocytes bound LFA-1+ T lymphocytes normally. Conjugate formation of activated LFA-1- T lymphocytes was mostly mediated by the CD2-LFA-3 adhesion pathway while the ICAM-1 molecule, a ligand of LFA-1, had no function. These results demonstrate that LFA-1 plays a major role in the cognate interaction between helper T lymphocytes and B lymphocytes that cannot be mediated instead by CD2 or other molecules on resting T lymphocytes.

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“…The inhibition of this blockage could result in a correction of a putative incapacity of these cells to express LFA-1. It should be noted here that activated T cells do express more LFA-1 than resting lymphocytes [11,24]. Likewise, this antigen is more abundant on macrophages activated by bacillus Calmette-Gu~rin or pyran copolymers than on resting ones [21].…”

Section: Discussionmentioning

confidence: 97%

“…As activated lymphocytes have been found to express greater amounts of LFA-1 than resting lymphocytes [24] and given the origin of MOLT-4 (a T-cell leukemia), we tested the ability of concanavalin A to induce the expression of LFA-1. Using two concentrations of this nonspecific mitogen, we succeeded in inducing a low level of LFA-1 on MOLT-4 surfaces ( Table 1).…”

Section: Attempts To Induce Lfa-1 Expression On Molt-4 Cellsmentioning

confidence: 99%

In vitro modulation of leucocyte-function-associated antigen-1 expression on two leukemic cell lines

Altmeyer

Moog

Waltzinger

et al. 1989

Cancer Immunol Immunother

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Leukocyte-function-associated antigen-1 (LFA-1) expression on two widespread tumor cell lines: K562 (an erythroleukemia) and MOLT-4 (a T leukemia), was investigated using two monoclonal antibodies specific for the alpha chain of this surface antigen, and flow cytometry analysis. When K562 cells are in the exponential phase of growth, they display very low levels of LFA-1. By contrast, cells from the plateau phase exhibit a strong labelling, which disappears rapidly when they are allowed to resume division by changing the culture medium. Using the same experimental conditions, we failed to detect any LFA-1 expression on MOLT-4 cells. However, after stimulation of these cells by phorbol myristate acetate, we observed a significant labelling, which occurred within 2 days of treatment. The LFA-1 expression disappears progressively after removal of the phorbol ester. From these results it may be concluded that (a) LFA-1 expression can vary considerably according to the culture conditions, (b) the expression of this antigen on the surface of non-expressing variants can be induced by phorbol ester, and (c) in both cases, the change in expression can be reversed completely by replacing the culture medium or by removing phorbol myristate acetate from it.

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Lymphocyte function-associated antigens one (LFA-1) on B and on T lymphocytes bind a monoclonal antibody with different affinities

Cited by 10 publications

References 21 publications

Deficiency of the adhesive protein complex lymphocyte function antigen 1, complement receptor type 3, glycoprotein p150,95 in a girl with recurrent bacterial infections. Effects on phagocytic cells and lymphocyte functions.

Deficiency of the adhesive protein complex lymphocyte function antigen 1, complement receptor type 3, glycoprotein p150,95 in a girl with recurrent bacterial infections. Effects on phagocytic cells and lymphocyte functions.

The role of lymphocyte function‐associated antigen 1 (LFA‐1) in the adherence of T lymphocytes to B lymphocytes

In vitro modulation of leucocyte-function-associated antigen-1 expression on two leukemic cell lines

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