scholarly journals Antiproliferative effect of antilymphocyte globulins on B cells and B- cell lines

Blood ◽  
1992 ◽  
Vol 79 (8) ◽  
pp. 2164-2170 ◽  
Author(s):  
N Bonnefoy-Berard ◽  
M Flacher ◽  
JP Revillard
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Immunosuppressive Agents ◽  
Lymphoproliferative Disorders ◽  
Hla Dr ◽  
T Cell Lines ◽  
Vitro Effect

Abstract Antithymocyte and antilymphocyte globulins (ALG) are currently used as immunosuppressive agents in organ transplantation and for the treatment of acute graft-versus-host disease and aplastic anemia. Since any type of immunosuppressive treatment is known to carry the risk of developing B-cell lymphoproliferative disorders, we investigated the in vitro effect of ALG on human B-cell activation and proliferation. The data demonstrate that whatever the source of lymphocytes used for ALG preparation (thymocytes, thoracic duct lymphocytes, B- or T-cell lines), (1) ALG react with both B- and T-cell lines, and (2) ALG contain antibodies specific for B cells (eg, CD21) or common to T and B cells (eg anti-beta 2-microglobulin, anti-HLA-DR, CD18, CD11a) in addition to T-cell-specific antibodies. Unlike all other T-cell mitogens tested (Concanavalin A [Con A], Pokeweek mitogen [PWM], CD3 and CD2 antibodies), ALG do not trigger B-cell differentiation into immunoglobulin-secreting cells at concentrations which induce maximum T- cell proliferation. This effect could be attributed to a direct interaction of ALG with B lymphocytes as shown by the capacity of ALG to block the response of purified B cells to a variety of activators. Furthermore, all the ALG tested were shown to inhibit the proliferation of six of the seven Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and six of the seven Burkitt's lymphoma cell lines studied. This selective B-cell antiproliferative property of ALG was not reproduced with CD11a, CD18, CD21, CD24, or anti-HLA-DR monoclonal antibodies (MoAbs). These results suggest that, although suppressing T- cell responses, ALG treatment may directly control B cell proliferation to some extent, in keeping with the relatively low risk of posttransplant lymphoproliferative disorders reported with ALG.

scholarly journals Antiproliferative effect of antilymphocyte globulins on B cells and B- cell lines

Blood ◽  
1992 ◽  
Vol 79 (8) ◽  
pp. 2164-2170
Author(s):  
N Bonnefoy-Berard ◽  
M Flacher ◽  
JP Revillard
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Immunosuppressive Agents ◽  
Lymphoproliferative Disorders ◽  
Hla Dr ◽  
T Cell Lines ◽  
Vitro Effect

Antithymocyte and antilymphocyte globulins (ALG) are currently used as immunosuppressive agents in organ transplantation and for the treatment of acute graft-versus-host disease and aplastic anemia. Since any type of immunosuppressive treatment is known to carry the risk of developing B-cell lymphoproliferative disorders, we investigated the in vitro effect of ALG on human B-cell activation and proliferation. The data demonstrate that whatever the source of lymphocytes used for ALG preparation (thymocytes, thoracic duct lymphocytes, B- or T-cell lines), (1) ALG react with both B- and T-cell lines, and (2) ALG contain antibodies specific for B cells (eg, CD21) or common to T and B cells (eg anti-beta 2-microglobulin, anti-HLA-DR, CD18, CD11a) in addition to T-cell-specific antibodies. Unlike all other T-cell mitogens tested (Concanavalin A [Con A], Pokeweek mitogen [PWM], CD3 and CD2 antibodies), ALG do not trigger B-cell differentiation into immunoglobulin-secreting cells at concentrations which induce maximum T- cell proliferation. This effect could be attributed to a direct interaction of ALG with B lymphocytes as shown by the capacity of ALG to block the response of purified B cells to a variety of activators. Furthermore, all the ALG tested were shown to inhibit the proliferation of six of the seven Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and six of the seven Burkitt's lymphoma cell lines studied. This selective B-cell antiproliferative property of ALG was not reproduced with CD11a, CD18, CD21, CD24, or anti-HLA-DR monoclonal antibodies (MoAbs). These results suggest that, although suppressing T- cell responses, ALG treatment may directly control B cell proliferation to some extent, in keeping with the relatively low risk of posttransplant lymphoproliferative disorders reported with ALG.

scholarly journals Interleukin 2 induces antigen-reactive T cell lines to secrete BCGF-I.

1983 ◽  
Vol 158 (6) ◽  
pp. 2024-2039 ◽  
Author(s):  
M Howard ◽  
L Matis ◽  
T R Malek ◽  
E Shevach ◽  
W Kell ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Interleukin 2 ◽  
Activated T Lymphocytes ◽  
T Cell Lines ◽  
Activated B Cells

Antigen-activated T lymphocytes produce within 24 h of stimulation a factor that is indistinguishable biochemically and functionally from the B cell co-stimulating growth factor, BCGF-I, originally identified in induced EL4 supernatants: Supernatants from antigen-stimulated T cell lines are not directly mitogenic for resting B cells, but synergize in an H-2-unrestricted manner with anti-Ig activated B cells to produce polyclonal proliferation but not antibody-forming-cell development; biochemical studies reveal the B cell co-stimulating factor present in antigen-stimulated T cell line supernatants is identical by phenyl Sepharose chromatography and isoelectric focusing (IEF) to EL4 supernatant BCGF-I. We thus conclude that normal T cells produce BCGF-I in response to antigenic stimulation. Analysis of the mechanism of BCGF-I production by antigen-stimulated T cells showed that optimum amounts of BCGF-I were obtained as quickly as 24 h post-stimulation, and that the factor producing cells in the T cell line investigated bore the Lyt-1+2- phenotype. As few as 10(4) T cells produced sufficient BCGF-I to support the proliferation of 5 X 10(4) purified anti-Ig activated B cells. Finally, the activation of normal T cell lines to produce BCGF-I required either antigen presented in the context of syngeneic antigen-presenting cells (APC) or interleukin 2 (IL-2).

scholarly journals Major histocompatibility complex-restricted, polyclonal B cell responses resulting from helper T cell recognition of antiimmunoglobulin presented by small B lymphocytes.

1985 ◽  
Vol 161 (1) ◽  
pp. 223-241 ◽  
Author(s):  
H P Tony ◽  
D C Parker
Keyword(s):  
Major Histocompatibility Complex ◽  
T Cell ◽  
B Cells ◽  
Cell Surface ◽  
B Cell ◽  
Cell Lines ◽  
Major Histocompatibility ◽  
Helper T Cell ◽  
Histocompatibility Complex ◽  
T Cell Lines

Anti-Ig has been widely used as a model for antigen receptor-mediated B cell activation. B cells activated with mitogenic concentrations of anti-Ig (approximately 10 micrograms/ml) become responsive to a set of T cell-derived, antigen-nonspecific helper factors that enable the B cells to proliferate, and, in some cases, mature to Ig secretion. In the present experiments, we show that anti-Ig can also be used as a model for major histocompatibility complex (MHC)-restricted, antigen-specific T-B cell collaboration. We used murine helper T cell lines and T cell hybridomas specific for a protein antigen, the F(ab')2 fragment of normal rabbit IgG. Small B cells are very efficient at presenting rabbit anti-IgM or rabbit anti-IgD to these rabbit Ig-specific T cell lines and hybridomas, and the responding (initially) small B cells, appear to be the only antigen-presenting cells required. Efficient presentation depends upon binding of rabbit antibody to mIg on the B cell surface. MHC-restricted recognition of rabbit Ig determinants on the B cell surface results in a polyclonal B cell response. This response is qualitatively different from the well-studied response to blastogenic concentrations of anti-Ig plus stable, T cell-derived helper factors, since it (a) requires 1,000-fold lower concentrations of anti-Ig, (b) involves helper T cell functions other than, or in addition to, the local production of the same stable helper factors, and (c) is largely MHC-restricted at the T-B cell level.

Splenic Macrophages Maintain the Anti-Platelet Autoimmune Response Via Uptake of Opsonized Platelets in Patients with Chronic ITP.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 221-221 ◽  
Author(s):  
Masataka Kuwana ◽  
Yutaka Kawakami ◽  
Yasuo Ikeda
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Cell Lines ◽  
Antibody Production ◽  
Tryptic Peptides ◽  
Splenic Macrophages ◽  
Hla Dr ◽  
T Cell Lines

Abstract ITP is an autoimmune disease mediated by autoantibodies to platelet membrane glycoproteins, such as GPIIb-IIIa. We recently identified CD4+ T cells reactive with GPIIb-IIIa in patients with chronic ITP, and these T cells are considered pathogenic because they help B cells produce antibodies that bind normal platelet surfaces in vitro. GPIIb-IIIa-reactive T cells respond to tryptic peptides of GPIIb-IIIa or recombinant GPIIb-IIIa fragments produced in bacteria, but not to native GPIIb-IIIa, indicating that the epitopes they recognized are ’cryptic’ determinants, generated at a subthreshold level by the processing of native GPIIb-IIIa under normal circumstances. We have found that activation of T cells and subsequent anti-platelet antibody production occur primarily in the spleen of ITP patients, but mechanisms that induce the processing and presentation of cryptic peptides of GPIIb-IIIa remains unknown. In this study, antigen-presenting cells (APCs) presenting the GPIIb-IIIa cryptic peptides was evaluated by their ability to induce a specific response of GPIIb-IIIa-reactive CD4+ T-cell lines generated from ITP patients undergoing splenectomy. All 6 T-cell lines used were HLA-DR-restricted Th0 cells with various antigenic specificity and 5 of them had helper activity. To identify splenic APCs responsible for presentation of the GPIIb-IIIa cryptic peptides, GPIIb-IIIa-reactive T-cell lines were cultured with freshly isolated autologous splenic APCs, including CD14+ macrophages, CD19+ B cells, or Lin−CD11c+ dendritic cells, in the presence or absence of GPIIb-IIIa tryptic peptides. All APCs induced a T-cell proliferation in response to the antigen. Interestingly, macrophages stimulated GPIIb-IIIa-reactive T-cell lines without any exogenous antigen, but B cells or dendritic cells did not. This response was blocked by anti-HLA-DR monoclonal antibody, indicating presentation of GPIIb-IIIa cryptic peptides by splenic macrophages in vivo in ITP patients. To further examine whether uptake of opsonized platelets by macrophages results in presentation of the GPIIb-IIIa cryptic peptides, GPIIb-IIIa-reactive T-cell lines were cultured with autologous macrophages, which were prepared by culturing peripheral blood monocytes with M-CSF, in the presence of platelets derived from ITP patients and healthy individuals. Cultured macrophages required preincubation of GPIIb-IIIa tryptic peptides to stimulate GPIIb-IIIa-reactive T-cell lines. As expected, cultured macrophages preincubated with autologous or allogeneic ITP platelets, but not with healthy platelets, were able to stimulate GPIIb-IIIa-reactive T-cell lines. A response of the T-cell line was also induced by macrophages carrying healthy platelets pre-treated with ITP platelet eluates. This response induced by macrophages carrying ITP platelets was completely inhibited by anti-FcγRI, but not by anti-FcγRII monoclonal antibody. Finally, GPIIb-IIIa-reactive T-cell lines failed to induce anti-GPIIb-IIIa antibody production in culture with autologous B cells and platelets, but anti-GPIIb-IIIa antibody production was observed when this culture was carried out on autologous macrophages. In summary, splenic macrophages are a source of the GPIIb-IIIa cryrptic peptides in ITP patients. It is likely that splenic macrophages that phagocytose opsonized platelets via FcγRI have the ability to efficiently concentrate small quantities of platelet antigens that were previously cryptic, and to maintain continuous production of pathogenic anti-platelet antibody.

scholarly journals CD4+ T-Cell Effectors Inhibit Epstein-Barr Virus-Induced B-Cell Proliferation

2001 ◽  
Vol 75 (8) ◽  
pp. 3740-3752 ◽  
Author(s):  
Sarah Nikiforow ◽  
Kim Bottomly ◽  
George Miller
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT In immunodeficient hosts, Epstein-Barr virus (EBV) often induces extensive B-cell lymphoproliferative disease and lymphoma. Without effective in vitro immune surveillance, B cells infected by the virus readily form immortalized cell lines. In the regression assay, memory T cells inhibit the formation of foci of EBV-transformed B cells that follows recent in vitro infection by EBV. No one has yet addressed which T cell regulates the early proliferative phase of B cells newly infected by EBV. Using new quantitative methods, we analyzed T-cell surveillance of EBV-mediated B-cell proliferation. We found that CD4+ T cells play a significant role in limiting proliferation of newly infected, activated CD23+ B cells. In the absence of T cells, EBV-infected CD23+ B cells divided rapidly during the first 3 weeks after infection. Removal of CD4+ but not CD8+ T cells also abrogated immune control. Purified CD4+ T cells eliminated outgrowth when added to EBV-infected B cells. Thus, unlike the killing of EBV-infected lymphoblastoid cell lines, in which CD8+ cytolytic T cells play an essential role, prevention of early-phase EBV-induced B-cell proliferation requires CD4+ effector T cells.

scholarly journals Interaction of helper T cells and Lyb5+ B cells responding to phosphorylcholine is MHC-restricted.

1984 ◽  
Vol 160 (1) ◽  
pp. 329-334 ◽  
Author(s):  
D E Mosier ◽  
A J Feeney
Keyword(s):  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Cell Subset ◽  
Keyhole Limpet Hemocyanin ◽  
Cell Subpopulation ◽  
Helper T Cell ◽  
T Cell Lines

The requirements for T cell/B cell interaction for the induction of primary in vitro antibody responses to phosphorylcholine (PC)-keyhole limpet hemocyanin (KLH) were examined. Long-term helper T cell lines derived from KLH-primed (CBA/N X BALB/c) F1 female mice (H-2k/d) were able to support a T15-idiotype dominant, IgM anti-PC response of BALB/c (H-2d) B cells and macrophages, but could not activate PC-specific responses by BALB.B (H-2b) B cells, even in the presence of irradiated H-2k/d antigen-presenting cells. Polyclonal IgM secretion in the same cultures did not appear to depend upon a major histocompatibility complex (MHC)-restricted T-B interaction. Since IgM anti-PC responses seem to be entirely derived from the Lyb5+ B cell subpopulation, we conclude that at least some Lyb5+ B cells can only be activated by MHC-restricted T-B interactions. We also found that xid B cells from (CBA/N X BALB/c) F1 male mice could be polyclonally activated by helper T cell lines by an apparently MHC-unrestricted interaction. Our data thus suggests that residence in the Lyb5- or Lyb5+ B cell subset does not determine the T:B interaction requirements for antibody synthesis.

scholarly journals T cell-derived B cell differentiation factor(s). Effect on the isotype switch of murine B cells.

1982 ◽  
Vol 155 (3) ◽  
pp. 734-748 ◽  
Author(s):  
P C Isakson ◽  
E Puré ◽  
E S Vitetta ◽  
P H Krammer
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Interleukin 2 ◽  
B Cell Differentiation ◽  
Differentiation Factor ◽  
T Cell Lines ◽  
Cell Differentiation Factor

Culturing BALB/c B cells for 6 d at low cell density in the presence of lipopolysaccharide (LPS) results in the appearance of a small number of IgG plaque-forming cells (PFC). The addition of supernatants from concanavalin A (Con A)-induced alloreactive (AKR anti-B6) long-term T cell lines (PK 7.1.1a and 7.1.2) or a T cell hybridoma (FS7-6.18) to LPS-treated B cells resulted in a marked increase in IgG PFC (3--10-fold higher than in cultures treated with LPS alone. The number of induced IgG PFC was not affected by removing IgG-bearing cells on the fluorescence-activated cell sorter, indicating that T cell-derived B cell differentiation factor enhances isotype switching of sIgG- cells, rather than selecting and expanding pre-existing subpopulations of sIgG+ cells. We also investigated the subclass of IgG produced in the absence or presence of T cell factors and found that PK 7.1.1a, PK 7.1.2, and FS7-6.18 supernatants selectively increased IgG1 production. Several other T cell supernatants containing a variety of lymphokines had no effect, suggesting that PK 7.1.1a, PK 7.1.2, and FS7-6.18 lines produce factor(s) that can specifically enhance the recovery of IgG secreting cells in culture in the presence of LPS. These factors, which we have termed B cell differentiation factors, are different from interleukin 1, interleukin 2, T cell-replacing factor, colony-stimulating factor, macrophage-activating factor, and immune interferon. Our results suggest that soluble factors produced by T cell lines and hybridomas can markedly influence both the class and subclass of Ig produced by B cells.

scholarly journals Antibody selection against CD52 produces a paroxysmal nocturnal haemoglobinuria phenotype in human lymphocytes by a novel mechanism

1997 ◽  
Vol 322 (3) ◽  
pp. 919-925 ◽  
Author(s):  
Vanessa C. TAYLOR ◽  
Martin SIMS ◽  
Sara BRETT ◽  
Mark C. FIELD
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Structural Gene ◽  
Biosynthetic Pathway ◽  
Human Lymphocytes ◽  
Paroxysmal Nocturnal Haemoglobinuria ◽  
T Cell Lines

The CD52 antigen is a lymphocyte glycoprotein with an extremely short polypeptide backbone and a single N-linked glycan, and it is attached to the cell membrane by a glycosylphosphatidylinositol (GPI) anchor. Treatment of rheumatoid arthritis patients with CAMPATH-1H, a humanized monoclonal antibody against CD52, resulted, in a small number of cases, in the appearance and persistence of CD52-negative T cells. Similarly, CD52-negative B cells emerged following in vitro treatment of a CD52-positive human B cell line with CAMPATH-1H. Both the B and T CD52-negative cells were also found to be defective in surface expression of other GPI-anchored proteins. Biochemical analysis revealed a severe defect in the synthesis of a mature GPI precursor in both the B and T cell lines. Therefore the phenotype of these CD52-negative B and T cells closely resembles that of lymphocytes from patients with paroxysmal nocturnal haemoglobinuria (PNH), in which the first step of the GPI-biosynthetic pathway, i.e. synthesis of GlcNAc-phosphatidylinositol, is blocked. In all cases studied to date, this defect maps to a mutation of the phosphatidylinositolglycan class A (PIG-A) structural gene. We therefore amplified the PIG-A gene from both the GPI-negative B and T cells by PCR and determined the nucleotide sequence. No differences from the wild-type sequence were detected; therefore a classical PNH mutation cannot be responsible for the GPI-biosynthesis defect in these cell lines. Significantly, the GPI-negative phenotype of the B cells was reversible upon separation of the positive and negative cells, resulting in a redistribution to a mixed population with either CD52-positive or -negative cells, whereas populations of 100% CD52-negative T cells were stably maintained during culture. Therefore, whereas the GPI-biosynthesis deficiency in the T cell lines may be due to a mutation in another gene required by the GPI-biosynthetic pathway, the reversible nature of this block in the B cell lines suggests a less direct cause, possibly an alteration in a regulatory factor. Overall, these data demonstrate that the PNH phenotype can be generated without a mutation in the PIG-A structural gene, and thereby identify a novel mechanism for the development of GPI deficiency.

scholarly journals Identification and Characterization of TspA, a Major CD4+ T-Cell- and B-Cell-StimulatingNeisseria-Specific Antigen

1999 ◽  
Vol 67 (7) ◽  
pp. 3533-3541 ◽  
Author(s):  
Goksel Kizil ◽  
Ian Todd ◽  
Mustafa Atta ◽  
S. Peter Borriello ◽  
Kamel Ait-Tahar ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Amino Acid ◽  
T Cell ◽  
Amino Acid Sequence ◽  
B Cell ◽  
Cell Lines ◽  
T Cell Proliferation ◽  
Significant Homology ◽  
T Cell Lines ◽  
Proliferation Assays

ABSTRACT In search for novel T-cell immunogens involved in protection against invasive meningococcal disease, we screened fractionated proteins of Neisseria meningitidis (strain SD, B:15:P1.16) by using peripheral blood mononuclear cells (PBMCs) and specific T-cell lines obtained from normal individuals and patients convalescing fromN. meningitidis infection. Proteins of iron-depleted meningococci produced higher PBMC proliferation indices than proteins of iron-replete organisms, indicating that iron-regulated proteins are T-cell immunogens. Insoluble proteins of the iron-depleted cells, which produced better T-cell stimulation than soluble ones, were fractionated by using sodium dodecyl sulfate-polyacrylamide gels and recovered as five fractions (F1 to F5) corresponding to decreasing molecular weight ranges. The proteins were purified (by elution and precipitation) or electroblotted onto nitrocellulose membranes (dissolved and precipitated) before use in further T-cell proliferation assays. One of the fractions (F1), containing high-molecular-mass proteins (>130 kDa), consistently showed the strongest T-cell proliferation responses in all of the T-cell lines examined. F1 proteins were subdivided into four smaller fractions (F1A to F1D) which were reexamined in T-cell proliferation assays, and F1C induced the strongest responses in patients’ T-cell lines. Rabbit polyclonal antibodies to F1C components were used to screen a genomic expression library of N. meningitidis. Two major clones (C1 and C24) of recombinant meningococcal DNA were identified and fully sequenced. Sequence analysis showed that C24 (1,874 bp) consisted of a single open reading frame (ORF), which was included in clone C1 (2,778 bp). The strong CD4+ T-cell-stimulating effect of the polypeptide product of this ORF (named TspA) was confirmed, using a patient T-cell line. Immunogenicity for B cells was confirmed by showing that convalescent patients’ serum antibodies recognized TspA on Western blots. Additional genetic sequence downstream of C24 was obtained from the meningococcal genomic sequence database (Sanger Centre), enabling the whole gene of 2,761 bp to be reconstructed. The DNA and deduced amino acid sequence data for tspA failed to show significant homology to any known gene, except for a corresponding (uncharacterized) gene in Neisseria gonorrhoeae genome sequences, suggesting that tspA is unique to the genusNeisseria. The DNA and deduced amino acid sequence of the second ORF of clone C1 showed significant homology to gloA, encoding glyoxalase I enzyme, of Salmonella typhimurium andEscherichia coli. Thus, we have identified a novel neisserial protein (TspA) which proved to be a strong CD4+T-cell- and B-cell-stimulating immunogen with potential as a possible vaccine candidate.

scholarly journals B cell-stimulatory factor 1 (BSF-1) promotes growth of helper T cell lines.

1986 ◽  
Vol 164 (2) ◽  
pp. 580-593 ◽  
Author(s):  
R Fernandez-Botran ◽  
P H Krammer ◽  
T Diamantstein ◽  
J W Uhr ◽  
E S Vitetta
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Activated T Cells ◽  
Growth Promoting ◽  
T Cell Lines ◽  
Stimulatory Factor

T cell-derived supernatants (SN) that contain B cell-stimulatory factor 1 (BSF-1) and lack IL-2 promote the growth of the IL-2-dependent T cell line, HT-2, as well as three other clones or lines of T cells that can provide help to B cells. The BSF-1 purified from these SNs promotes growth of HT-2 cells approximately 50% as effectively as purified IL-2. A potential involvement for contaminating IL-2 in the BSF-1 preparations was excluded by the demonstration that anti-BSF-1 mAbs blocked the BSF-1-induced growth of HT-2 cells; in contrast, these antibodies did not block the IL-2-induced proliferation of the HT-2 cells. In addition, anti-IL-2 mAbs or anti-IL-2-R antibodies blocked the HT-2 growth-promoting activity of purified IL-2, but not BSF-1. Finally, BSF-1 promoted only a very modest growth of Con A-induced T cell blasts, and failed to induce significant growth in seven other cytotoxic, alloreactive, and long-term T cell lines. Taken together, these results indicate that in addition to its known effects on resting and LPS-stimulated B cells, BSF-1 can promote growth of certain subsets of activated T cells, in particular, those that provide help to B cells.

Sign in / Sign up

Export Citation Format

Share Document