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Expression of the interleukin 2 receptor beta chain (p75) in renal transplantation--applicability of anti-interleukin-2 receptor beta chain monoclonal antibody.

The interaction of interleukin 2 with specific cellular receptors plays an essential role in the allostimulated proliferation and differentiation of T cells. Recent chemical linking studies have demonstrated that the human high-affinity IL-2 receptor is a membrane complex composed of at least two distinct subunits, which are the p55 (alpha-chain) and p75 (beta-chain) subunits. The IL-2R beta chain is supposed to play a role in the signal transduction of IL-2, but the exact mechanism is still unknown. In this study, we investigated the effects of a newly established anti-IL-2R beta chain monoclonal antibody (MoAb, TU-27) on the induction of cytotoxic T lymphocytes (CTLs) using the cell-mediated lympholysis (CML) assay. TU-27 in combination with H-31, a MoAb directed against the IL-2R alpha chain, produced inhibition of cytotoxicity, while TU-27 alone could not inhibit cytotoxicity, while TU-27 alone could not inhibit cytotoxicity at any concentration. TU-27 plus H-31 prevented the expansion of CD4+ cells and CD8++ cells in mixed lymphocyte culture (MLC). Furthermore, we examined the serial changes in the expression of the IL-2R beta chain on peripheral blood lymphocytes from renal transplant recipients using two-color immunofluorescence flow cytometry, so as to investigate correlations between IL-2R beta chain expression and the occurrence of allograft rejection. Here, we report that the IL-2R beta chain is expressed on CD4-positive (CD4+) cells and strongly CD8-positive (CD8(+)+) cells in association with acute rejection, indicating that IL-2R beta chain expression appears to increase on alloreactive T cells.

Antibodies, Monoclonal↗

Immunopathology of early graft-versus-host disease--a prospective study of skin, rectum, and peripheral blood in allogeneic and autologous bone marrow transplant recipients.

The immunopathological appearances of skin and rectum in 64 autologous and allogeneic recipients were determined before and after bone marrow transplantation. Patients who developed acute graft-versus-host disease were biopsied as soon as a clinical diagnosis was made. At the same time peripheral blood samples were collected for comparative analysis. Immunohistological and morphometric techniques were employed using a panel of monoclonal antibodies to T lymphocytes and subsets, B lymphocytes, natural killer cells, macrophages, and Langerhans cells. A reduction in the CD4/CD8 ratio after BMT was seen in skin and rectal biopsies from both autologous and allogeneic recipients with or without GVHD. The same pattern was observed in blood samples taken at the same time. Langerhans cells were reduced in the skin in all patients after BMT, probably by the conditioning regimen. Only a few cells expressing activation or natural killer cell markers were present and there were no changes observed in the macrophage population. This study has provided no evidence to implicate either CD4- or CD8-positive T lymphocytes as the initiators of the cellular damage in acute GVHD. The distribution of lymphocyte subsets in the blood was similar to that in the tissues, suggesting that the tissue changes reflect the pattern of lymphocyte repopulation after BMT and may have little bearing on the pathogenesis of GVHD.

Adolescent↗

HLA-Bw54-DR4-DRw53-DQw4 haplotype controls nonresponsiveness to hepatitis-B surface antigen via CD8-positive suppressor T cells.

We have previously reported that in nonresponders to hepatitis-B (HB) vaccine there was an HLA-linked immune suppression gene for hepatitis-B surface antigen (Is-HBsAg) controlling the nonresponsiveness to HBsAg, through HBsAg-specific suppressor T cells, and that the Is-HBsAg was in strong linkage disequilibrium with the HLA-Bw54-DR4-DRw53 haplotype (1). We have now done the HLA typing on an additional 6 nonresponders, and using the system of T-cell proliferative response to HBsAg we found that the Is-HBsAg controlled the nonresponsiveness to HBsAg through HBsAg-specific suppressor T cells in nonresponders to HB vaccine who have HLA-Bw54-DR4-DRw53-DQw4 haplotype. T- and B-cell recognition of HB vaccines might play an important role at 3 to 5 weeks after the last immunization. Use of an anti-HLA monoclonal antibody has shown that the HLA-DR molecule plays an important role in helper T-cell proliferation in nonresponders, although the role of HLA-DQ molecule in nonresponders was unclear.

Antibodies, Monoclonal↗

Expression of CD31 epitopes on human lymphocytes: CD31 monoclonal antibodies differentiate between naive (CD45RA+) and memory (CD45RA-) CD4-positive T cells.

The CD31 antigen, a member of the immunoglobulin superfamily with a possible cell adhesion function, is expressed on approximately 50% of peripheral blood lymphoid cells at relatively low intensity (10-20% of the level on monocytes). In the accompanying paper we showed that a mAb, 5A2.G5, which identifies a glycosylation-dependent epitope of the CD31 antigen, bound to fewer lymphocytes than two other CD31 mAb, B2B1 and 2BD4, although the 3 antibodies bound equally well to monocytes. We have now analyzed the pattern of expression of epitopes of the CD31 antigen on lymphoid cell subpopulations using two-color immunofluorescence and flow cytometry. Large granular lymphocytes (CD16+), CD8-positive T cells and B cells (SMIg+) were mostly CD31-positive as indicated by the binding of mAb B2B1 and 2BD4. Single populations displaying some overlap with the negative control were obtained in each case. In contrast, CD4-positive T cells fell into two discrete populations with respect to CD31 antigen expression. mAb 5A2.G5 displayed weaker binding to all lymphoid cell types, indicating that the pattern of glycosylation of the CD31 antigen differs between lymphocytes (of all types) and cells of the myeloid lineages. The heterogeneity of CD31 antigen expression by CD4-positive cells was further examined by dual-labelling of purified CD4 cells with mAb B2B1 and CD45RA or CD29 mAb which identify naive and memory T cells respectively. The CD31 antigen was found to be preferentially expressed by the CD45RA-positive, naive cell population.

Antibodies, Monoclonal↗

Diversity of Francisella tularensis antigens recognized by human T lymphocytes.

The Francisella tularensis T-lymphocyte antigens, which may have a role in protection against tularemia, were investigated with vaccine-immunized subjects. Preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) was used to fractionate the bacterial envelope preparation. The 23 fractions obtained represented membrane proteins of different apparent molecular masses ranging from 10 to 150 kilodaltons. Different fractions contained one to four separate protein bands stained with Coomassie blue. The lymphocyte blast transformation responses of five tularemia vaccine-immunized and three nonimmunized subjects were tested against bacterial material eluted out of SDS-PAGE fractions. Every fraction stimulated lymphocytes from at least one of the subjects. No clearly immunodominant or inhibitory antigens were detected among the envelope fractions. Expression of the HLA-DR antigen at the surface of CD4- and CD8-positive lymphocytes was also studied as a measure of cell activation. The numbers of CD4+ DR+ cells varied directly with the lymphocyte proliferation profiles, and very few CD8+ cells were found in the preparations stimulated with the different fractions. The diversity of the antigens recognized by immune T lymphocytes was confirmed by using F. tularensis-specific T-lymphocyte clones obtained from vaccinated subjects. Most of the 36 T-lymphocyte clones tested were stimulated by one SDS-PAGE fraction only.

Antigens, Bacterial↗

Impaired autologous mixed-lymphocyte reaction of peripheral blood lymphocytes in adult periodontitis.

The autologous mixed-lymphocyte reactions (AMLR) of peripheral blood lymphocytes from 80 patients with adult periodontitis were examined. Some but not all patients showed clearly low AMLR responses; 31 of 80 subjects (39%) showing consistently low responses in AMLR (less than the mean--2 standard deviations of the healthy control group values) were designated low-AMLR patients, whereas the 42 patients (53%) who showed normal AMLR responses were designated normal-AMLR patients. However, there were no significant differences in the clinical parameters between these two groups of patients. The phenotypic analysis of T-cell fractions revealed a lower percentage of CD45RA-positive cells in CD4-positive cells (CD4+ CD45RA+ T cells) in the low-AMLR patients than those in normal-AMLR patients and healthy control subjects. No significant differences were demonstrated between the two groups in terms of the proportion of CD4-positive and CD8-positive cells in the T-cell fractions or in the expression of human leukocyte antigen DR of the monocytes and B cells in the non-T-cell fractions. In the low-AMLR patients, the allogeneic MLR was found to be normal, but the interleukin 2 production in the AMLR was found to be significantly depressed. The depressed AMLR responses and the lower percentage of CD4+ CD45RA+ T cells in the low-AMLR patients were found to be normalized following the periodontal therapy. These results might reflect changes in regulatory T-cell function induced by development of periodontal diseases.

Adult↗

Role and specificity of T-cell subsets in spontaneous recovery from Friend virus-induced leukemia in mice.

Spontaneous recovery from Friend virus complex-induced leukemic splenomegaly in H-2Db/b mice correlated with the appearance of Friend virus complex-specific cytotoxic T lymphocytes (CTL) detectable directly in spleen cell populations. By testing CTL on target cells containing expression vectors encoding individual retroviral structural proteins, the main viral protein recognized was shown to be the Friend murine leukemia helper virus envelope glycoprotein. In vivo depletion of CD8-positive T cells drastically reduced the incidence of recovery, providing direct evidence for the role of CD8-positive CTL in the spontaneous recovery process. In vivo depletion of CD4-positive cells had little effect on the early stages of recovery but did cause a marked reduction in the final incidence of recovery at 60 to 90 days. Thus, CD8-positive cells were required for the initiation of the recovery process, whereas CD4-positive cells appeared to be required for maintenance of the recovered status.

Animals↗

Effect of glycyrrhizin on pain and HLA-DR antigen expression on CD8-positive cells in peripheral blood of herpes zoster patients in comparison with other antiviral agents.

Glycyrrhizin (GL) is a saponin widely used as an anti-inflammatory agent. Pain intensity and HLA-DR antigen expression on CD8+ cells were assessed during and after treatment with GL. Other agents such as acyclovir, gamma-globulin and interferon beta were also administered for comparison. Pain resolved most rapidly among those treated with acyclovir followed by those treated with GL. Pain resolution correlated with the regression of HLA-DR+ in CD8+ subpopulations in peripheral blood. GL is suggested to be an alternative or additive antiviral agent to herpes zoster.

Acyclovir↗

Complement receptor type 1 (CR1, CD35) expression on peripheral T lymphocytes: both CD4- and CD8-positive cells express CR1.

T lymphocytes from 42 healthy blood donors were examined for expression of CR1 on the cell surface using a fluorescence-activated cell sorter. The fraction of CR1-positive T lymphocytes varied in the range from 1 to 8% (median 2.4%). The CR1-positive T lymphocytes constituted a homogeneous group of cells regarding both size and granulation; they seemed to be larger and more granulated than the average T lymphocytes. The CR1-expressing T lymphocytes were found both in the CD4- and in the CD8-positive subpopulations of T lymphocytes, and although the CD4-positive cells expressed CR1 with a slightly higher percentage than did the CD8-positive cells, this difference was not significant. The number of CR1-positive T lymphocytes did not correlate with the level of CR1 on erythrocytes. The presence of CR1 on a small T lymphocyte population suggests that CR1 on T lymphocytes might play a role in the immune regulation.

Antigens, Differentiation, T-Lymphocyte↗

Distribution of lymphoid cells in tonsillar compartments in relation to infection and age. A quantitative study using image analysis.

The distribution of lymphoid cells in the mantle zone, germinal center, interfollicular area, and subepithelial area of the tonsil was evaluated quantitatively by image analysis in 66 subjects aged 3 to 66 years. The number of Ig-positive cells in the tonsil decreased with advancing years in all compartments. This inverse correlation to age was statistically significant for IgD-, IgM-, and IgG-positive cells. For T-cells, overall change of each T-cell subset with age was smaller than those of Ig-positive cells. An age-related marked decline was seen for CD4-positive cells only in the subepithelial area and for CD8-positive cells only in the interfollicular area. Ki-67-positive cells, cells undergoing active division, were mainly found in the germinal centers and also diminished with advancing years. Patients with frequent episodes of tonsillitis demonstrated a significant increase of IgD-positive cells and IgG-positive cells in interfollicular and subepithelial compartments and a decrease of CD4-positive T-cells in the germinal centers and subepithelial areas. These results suggest that the tonsillar involution with age is immunologically associated in all compartments with the decrease of Ig-positive cells and Ki-67-positive activated cells resulting in a relative increase of T-cell subsets. The method of image analysis provides a novel and unique approach for quantitative immunohistological study of the tonsil.

Adolescent↗

Analysis of the mechanism of graft-versus-host-like disease in B6 mice with transferred B6-lpr spleen cells.

Irradiated C57BL/6(B6) mice, when they were injected with spleen cells of C57BL/6J-lpr/lpr(B6-lpr) mice, developed splenomegaly at 2 weeks post-transfer, but afterward displaced by GVH-like disease. At 2 weeks the enlarged spleen in the chimeric mice, designated as [B6-lpr----B6] chimera, contained about 70% of the total cell population as CD8-positive T cells. Spleen cells from [B6-lpr----B6] chimeras were unresponsive to Con A and LPS stimulation and suppressed the mitogenic response of B6, B6-lpr, and C3H spleen cells to Con A. However, they had no cytotoxic activity towards Con A blasts of B6 and B6-lpr spleen cells. The suppressor activity found in the [B6-lpr----B6] spleen cells was removed by pretreatment of them with anti-Thy-1.2 or anti-CD8(Lyt2.2) plus complement. The present experiment showed that enormous proliferation of CD8-positive suppressor T cells was induced in the [B6-lpr----B6] chimeras. These cells were probably responsible for the GVH-like lymphoid atrophy observed in these [B6-lpr----B6] chimeras.

Animals↗

Intrahepatic lymphocyte subpopulations and HLA class I antigen expression by hepatocytes in chronic hepatitis C.

The lymphocyte subpopulations in the peripheral blood and liver were studied in 17 patients with chronic active hepatitis type C (CAH C) by immunoenzymatic and immunofluorescence techniques, using mono-specific T cell antibodies and other reagents. The peripheral blood subsets showed no significant differences between the patients with CAH C and normal controls. In the liver, CD8-positive cells were predominant over CD4- and Leu 7-positive cells. Leu 7-, CD4-, and CD11-positive lymphocytes were all few in number. HLA class I antigen was expressed diffusely on the cell surfaces of the hepatocytes. Serum levels of soluble interleukin 2 receptor (sIL2R) in the CAH C patients were significantly higher than in normal controls (p less than 0.01). In CAH C, sIL2R levels were higher during exacerbations than during remissions (p less than 0.01). These results suggest that cytotoxic T cells (CD8- positive, CD4-negative, and CD11-negative) may play an important role in the pathogenesis of hepatocyte injury in patients with CAH C.

Antibodies, Monoclonal↗

The HML-1 antigen of intestinal lymphocytes is an activation antigen.

The Ag recognized by the mAb HML-1 is expressed on more than 90% of human intestinal intraepithelial lymphocytes, whereas in other lymphoid tissues it is rarely or not expressed. In the present study, we have investigated the percentage of HML-1-positive cells in the human intestinal lamina propria and the coexpression of HML-1 with different T cell subset markers. In addition, we studied the inducibility of HML-1 on PBL which normally are HML-1-negative. Flow cytometric analysis of isolated intestinal lamina propria lymphocytes (LPL) showed that about 40% of the cells expressed HML-1, the majority belonging to the CD8-positive subpopulation. Virtually all LPL expressed CD45RO, whereas the percentage of CD29-positive cells was only about 50%, similar to PBL. There were only few cells expressing CD45RA or Leu-8 in the lamina propria. HML-1-positive cells were almost exclusively CD45RA-negative, but were found in both the CD29-positive and the CD29-negative subpopulation of LPL. In vitro stimulation of PBL showed that the expression of HML-1 was inducible on T cells by mitogens, phorbolester, Ag, and rIL-2. Expression of HML-1 was induced with a different time course and with differences in the response to the investigated stimuli compared with CD25. Activated HML-1-positive PBL were also predominantly CD45RA-negative. The findings show that HML-1 is an Ag, which is expressed in vivo on a specific subset of previously activated T cells in the unique environment of the intestinal mucosa, and which can be induced in vitro by different activation signals on PBL.

Antibodies, Monoclonal↗

Hepatitis B surface antigen-specific CD8-positive T cell clones. Antigen specificity and interleukin-2 production.

Clones of hepatitis B surface antigen-reactive CD8+ and CD4+ T cells were obtained from peripheral blood mononuclear cells (PBM) of a hepatitis B immunized individual whose PBM proliferated when cultured with hepatitis B surface antigen (HBsAg). Lymphocytes were activated by culturing for 2 weeks with HBsAg and high concentrations of interleukin-2 (IL-2), then cloned in the presence of irradiated HBsAg-activated PBM and autologous Epstein-Barr virus (EBV)-transformed B cells, together with antigen and IL-2. All clones examined proliferated in an antigen-specific manner. Of 7 clones examined by flow cytometry, 4 were CD4+, CD8-; and 3 were CD4-, CD8+. Several clones produced IL-2 activity after stimulation with hepatitis B surface antigen. Since development of CD8+ T-cell clones specific for soluble antigens is difficult, the high frequency with which CD8+ cells were cloned in these experiments suggests that the cloning strategy employed might have general use for development of CD8+ clones. Availability of hepatitis B virus specific T cell clones of different phenotypes may help elucidate mechanisms of immunotolerance in hepatitis B infection.

CD4-Positive T-Lymphocytes↗

Human abdominal aortic aneurysms. Immunophenotypic analysis suggesting an immune-mediated response.

Cellular immunity may play a role in the pathogenesis of atherosclerosis. In this report the potential role of these cells in the formation of abdominal aortic aneurysms by immunohistochemistry was investigated. Aortic tissues from 32 patients were examined: 4 normal aortas, 6 aortas with occlusive atherosclerotic disease, 17 abdominal aortic aneurysms, and 5 inflammatory abdominal aneurysms. Using monoclonal anti-CD3 (T cells), anti-CD19 (B cells), anti-CD11c (macrophages), anti-CD4 (T helper cells), and anti-CD8 (T suppressor cells), several distinctions among these groups were found. The amount of inflammatory cell infiltrate was as follows: inflammatory aneurysms more than abdominal aortic aneurysms more than occlusive aortas more than normal aortas. CD3-positive T lymphocytes rarely were found in the adventitia of normal or occlusive aortas. In contrast, abdominal aortic aneurysms and inflammatory aneurysms exhibited most of the CD3-positive infiltrates in the adventitia. CD19-positive B lymphocytes were present mainly in the adventitia of all pathologic tissues. The CD4-positive:CD8-positive ratio was greater in abdominal aortic aneurysms and inflammatory aneurysms than in the other groups, both in the adventitia and in the media of the aortas. CD11c-positive macrophages were present throughout the diseased tissues, often surrounded by lymphoid aggregates; the greatest numbers of macrophages were found in the inflammatory aneurysm group. Our data suggests that the aneurysmal disease may progress from occlusive disease and is accompanied by an increase in chronic inflammatory cells as well as a redistribution of these cell types. Therefore it is suggested that aneurysmal disease may represent an immune-mediated event.

Antibodies, Monoclonal↗

Primary proliferative and cytotoxic T-cell responses to HIV induced in vitro by human dendritic cells.

In earlier studies, primary proliferative and cytotoxic T-cell (CTL) responses to influenza virus were produced in vitro by using mouse dendritic cells (DC) pulsed with virus or viral peptide as the stimulus for syngeneic T cells in 20-microliters hanging-drop cultures. We have now adapted this system for producing primary responses with cells from non-immune donors to produce primary proliferative and CTL responses to human immunodeficiency virus I (HIV) and to HIV peptides in vitro using cells from normal human peripheral blood. All donors in this study were laboratory personnel with no history of HIV infection. DC enriched from peripheral blood were exposed to HIV in vitro and small numbers were added to T lymphocytes in 20-microliters hanging drops. Proliferative responses to virus-infected DC were obtained after 3 days in culture. After 6 days, CTL were obtained that killed virus-infected autologous--but not allogeneic--phytohaemagglutinin (PHA)-stimulated blast cells. Proliferative and CTL responses were obtained using cells from 14 random donors expressing a spectrum of major histocompatibility complex (MHC) types but the CTL, once produced, showed killing restricted by the MHC class I type. Treatment of cultures with monoclonal antibody (mAb) to CD4-positive cells at the beginning of culture blocked the development of both proliferative and CTL responses, but treatment after 5 days had no effect on the CTL activity. Treatment with MCA to CD8-positive cells at the beginning of culture did not block proliferation significantly, but treatment either before or after the 5-day culture period blocked CTL responses. Collaboration between proliferating CD4-positive cells and CD8-positive cells may thus be required to produce CTL of the CD8 phenotype. DC exposed to HIV also produced CTL that killed autologous blast cells pulsed with gp120 envelope glycoprotein. However, DC infected with whole virus did not produce CTL that lysed target cells pulsed with a synthetic peptide, which included a known T-cell epitope of gp120 (representing amino acids 111-126). DC pulsed with gp120 were a poor stimulus for the development of CTL. In contrast, DC pulsed with the peptide (111-126) stimulated both proliferative and CTL responses. The latter killed not only target cells pulsed with the peptide itself or with gp120 but also killed virus-infected autologous blast cells. CTL were again obtained reproducibly with this peptide using donors expressing a spectrum of MHC types.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell Division↗

Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients.

To investigate whether autoantibodies against CD4-positive lymphocytes might induce helper dysfunction, autoantibody formation and T-cell function was examined simultaneously in 61 hemophilia patients. Twenty patients were human immunodeficiency virus (HIV)-negative, 26 HIV-positive stage CDC II or III, and 15 were HIV-positive stage CDC IV. T lymphocytes, CD4-positive, or CD8-positive T subsets were cocultured with B lymphocytes and pokeweed mitogen (PWM) for 6 days and Ig-secreting cells were assessed in a reverse hemolytic plaque assay. The presence of IgM, IgG, C3d, or gp120 on the surface of T cells or T subsets was analyzed by flow cytometry. Autoantibodies against CD4-positive T cells were not detected in controls or HIV-negative patients, but were common in HIV-positive patients (20 of 41 patients). In patients with autoantibodies we found an increased incidence of CD4 helper defects (P less than .0001 in CDC II or III patients; P less than .02 in CDC IV patients). 12 of 13 patients with IgM autoantibodies and 4 of 4 with IgG autoantibodies showed CD4 helper defects. Complement fixation had no relevance. Autoantibody formation against CD4 cells was not due to increased in vivo B-cell stimulation (spontaneous plaque formation: 611 +/- 204 PFC/10(6) B cells in autoantibody-negative patients v 650 +/- 202 PFC/10(6) B cells in autoantibody-positive patients; not significant). Thus, our results suggest that autoantibody formation is not caused by a general state of in vivo B-cell activation. Rather, the production of autoantibodies appears to coincide with defects in B-cell proliferation or differentiation, as shown by reduced mitogen-stimulated B-cell responses in CDC II and III patients (P less than .05). Autoantibodies against CD4 cells appear to be involved in the pathogenesis of CD4 helper defects of HIV-infected patients.

Antigens, CD↗

Differential regulation of fibronectin receptor subunit gene and cell surface expression in human peripheral blood T lymphocytes.

Members of the beta 1 subfamily of heterodimeric integrins, such as the fibronectin receptors alpha 5 beta 1 and alpha 4 beta 1, are expressed on human T lymphocytes. The presence of these two adhesion receptors on T lymphocytes suggests an involvement in cell-cell and cell-extracellular matrix interactions that may be important for the development of immune and inflammatory reactions. We have examined the cell surface expression of alpha 5, alpha 4, and beta 1 subunits on purified peripheral blood T lymphocytes before and after activation with Con A and PMA. Freshly isolated T lymphocytes contained distinct fractions expressing high or low levels of alpha 5 and beta 1. Only a high expressing T lymphocyte population was present after 72-h culture with Con A and PMA. Time course analysis indicated that the shift in alpha 5 and beta 1 expression occurred during the first 24 h after addition of activating agents and occurred in the absence of proliferation. In contrast to alpha 5 and beta 1, essentially all freshly isolated T lymphocytes expressed high levels of alpha 4. After 72-h culture with Con A and PMA, a wide distribution of alpha 4 expression was observed. Further experiments showed that after activation, a proportion of CD4-positive cells decreased their surface expression of alpha 4, but increased their surface expression of alpha 5 and beta 1. In contrast, most CD8-positive cells increased their surface expression of alpha 5, beta 1, and alpha 4 upon activation. An examination of mRNA levels in pan-T lymphocyte cultures after activation indicated that alpha 5 and alpha 4 mRNA expression decreased, whereas beta 1 mRNA expression was unchanged, in Con A/PMA-activated cells as compared to those cultured in medium alone. Our results indicate that T lymphocyte activating agents may differentially affect the expression of alpha 5 beta 1 and alpha 4 beta 1, thus providing a mechanism for the selective regulation of binding interactions that occur at sites of immune reactions.

Concanavalin A↗