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PubMed1983

Phorbol ester modulation of T-cell antigens in the Jurkat lymphoblastic leukemia cell line.

The effect of phorbol dibutyrate (PDB) on the cell surface antigens of the human T-cell acute lymphoblastic leukemia cell line, Jurkat, was studied with OKT monoclonal antibodies by indirect immunofluorescence assay. Cells were analyzed in an Ortho Spectrum III fluorescence-activated flow cytometer. The surface antigen profile of untreated Jurkat cells resembled that of thymocytes; high levels of T3, T4, T6, T8, T9, T10, and T11 antigens were detected. Although 89% of cells were positive for T11, the putative sheep erythrocyte receptor, only 12% were able to form erythrocyte (sheep) rosettes. Exposure of the cells to 1.0 microM PDB for up to 7 days resulted in a rapid loss in T4 expression and a slower decrease in T6 reactivity, while the percentage of cells positive for T3, T8, T10, and T11 remained high. T4 reappeared on the cell surface when PDB was removed by washing. T11 antigen density increased 70%, and this was accompanied by an increase in the percentage of erythrocyte-rosetting cells from 12 to 55%. These changes in cell surface antigens induced by PDB suggested differentiation to a more mature state (i.e., a precursor cytotoxic-suppressor T-lymphocyte, T3+T8+T10+T11+). However, the reversibility of the change in T4 expression indicated that T4 loss was not a manifestation of terminal differentiation but rather was consistent with a phorbol ester-induced modulation of the cell surface T4 antigen.

Antigens, Surface↗
PubMed2006

Carcinoembryonic antigen-related cell adhesion molecule 1 modulates vascular remodeling in vitro and in vivo.

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), a cellular adhesion molecule of the Ig superfamily, is associated with early stages of angiogenesis. In vitro, CEACAM1 regulates proliferation, migration, and differentiation of murine endothelial cells. To prove that CEACAM1 is functionally involved in the regulation of vascular remodeling in vivo, we analyzed 2 different genetic models: in Ceacam1-/- mice, the Ceacam1 gene was deleted systemically, and in CEACAM1(endo+) mice, CEACAM1 was overexpressed under the control of the endothelial cell-specific promoter of the Tie2 receptor tyrosine kinase. In Matrigel plug assays, Ceacam1-/- mice failed to establish new capillaries whereas in CEACAM1(endo+) mice the implants were vascularized extensively. After induction of hind limb ischemia by femoral artery ligation, Ceacam1-/- mice showed significantly reduced growth of arterioles and collateral blood flow compared with their WT littermates. In agreement with a causal role of CEACAM1 in vascular remodeling, CEACAM1(endo+) mice exhibited an increase in revascularization and collateral blood flow after arterial occlusion. Our findings indicate that CEACAM1 expression is important for the establishment of newly formed vessels in vivo. Hence CEACAM1 could be a future target for therapeutic manipulation of angiogenesis in disease.

Animals↗
PubMed1999

Modulation of HLA-DR antigen and ICAM-1 molecule expression on airway epithelial cells by sodium nedocromil.

OBJECTIVE: To test in vitro and in vivo the hypothesis that sodium nedocromil could modulate the expression of surface molecules on airway epithelial cells. METHODS: Human bronchial epithelial cells, obtained from surgically resected bronchi, were cultured and stimulated with recombinant IFN-gamma in the presence of sodium nedocromil. The intensity of the expression of surface molecules HLA-DR and ICAM-1 molecules on bronchial epithelial cells in vitro, was quantified by specific antibody staining and flow-cytometry analysis. Furthermore, we studied the effect of the drug on airway inflammation in vivo and on allergic rhinitis patients sensitized to house dust mites. Nasal epithelial cells were collected by brushing, at baseline and 2 to 3 weeks after treatment with sodium nedocromil. The expression of HLA-DR and ICAM-1 molecules was measured by flow-cytometry, and the proportions of neutrophils and eosinophils "contaminating" the epithelial cells evaluated by light microscopy examination of nasal brushings. RESULTS: The enhanced HLA-DR and ICAM-1 expression, induced by IFN-gamma, was effectively downregulated, in a dose-dependent manner, by sodium nedocromil. At all the concentrations tested (10(-9) to 10(-4) M), the inhibitory activity of the drug was stronger on HLA-DR than on ICAM-1 expression (P<.05, all comparisons). As compared with healthy subjects, patients with allergic rhinitis had a higher expression of HLA-DR (P<.05) but not of ICAM-1 molecules (P>.05) on nasal epithelial cells, and higher proportions of nasal eosinophils (P<.05). Treatment with sodium nedocromil downregulated the expression of HLA-DR (P<.05), but not of ICAM-1 (P>.05), and induced a mild, but not statistically significant, decrease of nasal eosinophilia (P>.05). CONCLUSION: These data demonstrate that the antiinflammatory activity of sodium nedocromil may include modulation of surface molecule expression on airway epithelial cells.

Adolescent↗
PubMed1994

MHC antigen presentation on the surface of hepatocytes: modulation during and after hypoxic stress.

Presentation and recognition of MHC antigen on the surface of cells is the basic process of initiating rejection and distinguishing "self and not self". This is considered to begin when a transplanted organ is reperfused with the blood of the recipient. In this study, the modulation of MHC I antigen presentation during preservation was investigated in a cell culture model using primary hepatocyte cultures of male Wistar rats. By incubation with different preservation solutions used in clinical transplantation, expression of the MHC antigen was observed during cold hypoxia. Primary hepatocyte cultures were isolated from male Wistar rats by a modified Seglen technique and seeded to glass slides, thus obtaining monolayer cultures. After 1 day of resting the cultures were incubated under different conditions using Krebs Henseleit solution (KH), Euro-Collins solution (EC), HTK solution of Bretschneider (HTK) and University of Wisconsin solution (UW) as incubation media. The conditions of incubation were warm normoxia (37 degrees C, pO2 100 mm Hg) and cold hypoxia (4 degrees C, pO2 < 0.1 mm Hg), which is the main condition of organ preservation. Incubation time was 6 h. Before starting the incubation reference cultures were fixed and every 60 min several cultures were withdrawn from the experiment and fixed also. MHC expression was studied by staining the cultures with monoclonal antibodies against rat MHC class I and class II. As expected, MHC class II was not present on the surface of hepatocytes, while MHC class I was demonstrated on the controls as well as on the cultures that were incubated using KH and EC independent of temperature and hypoxia or normoxia. At the end of the incubation they were still positive but not as strong as in the beginning. During incubation using HTK and UW, MHC I was not detectable at all phases of the experiment. In conclusion, hypoxic stress did not completely eradicate MHC I expression in rat hepatocytes, while the composition of the preservation medium may result in a hepatocyte surface negative for MHC I. Hydroxyethylstarch may be the substance in UW that covers the MHC antigen, while in HTK, mannitol or the histidine complex may play the same role. MHC negativity of the cells of a preserved transplant is another reason for the benefit of UW or HTK.

Animals↗
PubMed1997

Immunologic tolerance to myelin basic protein decreases stroke size after transient focal cerebral ischemia.

Immune mechanisms contribute to cerebral ischemic injury. Therapeutic immunosuppressive options are limited due to systemic side effects. We attempted to achieve immunosuppression in the brain through oral tolerance to myelin basic protein (MBP). Lewis rats were fed low-dose bovine MBP or ovalbumin (1 mg, five times) before 3 h of middle cerebral artery occlusion (MCAO). A third group of animals was sensitized to MBP but did not survive the post-stroke period. Infarct size at 24 and 96 h after ischemia was significantly less in tolerized animals. Tolerance to MBP was confirmed in vivo by a decrease in delayed-type hypersensitivity to MBP. Systemic immune responses, characterized in vitro by spleen cell proliferation to Con A, lipopolysaccharide, and MBP, again confirmed antigen-specific immunologic tolerance. Immunohistochemistry revealed transforming growth factor beta1 production by T cells in the brains of tolerized but not control animals. Systemic transforming growth factor beta1 levels were equivalent in both groups. Corticosterone levels 24 h after surgery were elevated in all sham-operated animals and ischemic control animals but not in ischemic tolerized animals. These results demonstrate that antigen-specific modulation of the immune response decreases infarct size after focal cerebral ischemia and that sensitization to the same antigen may actually worsen outcome.

Animals↗
PubMed1991

Lipopolysaccharide from Escherichia coli reduces antigen-induced bronchoconstriction in actively sensitized guinea pigs.

Bronchoconstriction (BC) is the main feature of anaphylaxis in the guinea pig. Since LPS induces lung inflammation and antigen-induced BC depends on the endogenous formation of histamine and arachidonate metabolites, we studied whether LPS might modulate antigen-induced BC. Guinea pigs were sensitized subcutaneously with 10 micrograms ovalbumin (OA) on days 0 and 14. LPS (100 micrograms/kg) was injected intravenously on day 21, and daily injections of LPS were continued before the antigenic challenge on day 22, 23, 24, or 25. Intratracheal injection of 100 micrograms OA induced an abrupt and reversible BC. Single or repetitive injections of LPS reduced BC. LPS is likely to reduce the OA-induced BC by affecting the histamine-dependent component of BC, since (a) LPS induced a partial degranulation of lung mast cells; (b) BC is reduced by mepyramine, an histamine receptor antagonist; (c) LPS did not affect BC in mepyramine-treated guinea pigs; (d) LPS reduced histamine release by OA-stimulated guinea pig lungs in vitro. Moreover, the in vitro OA-induced production of arachidonate metabolites was also reduced by LPS. The decreased formation of TXB2 was not only secondary to a reduced release of histamine, since LPS inhibited TXB2 formation in the presence of mepyramine. Finally, the FMLP-induced BC and mediator release were inhibited by LPS, whereas the platelet activating factor-induced pulmonary responses were not. Thus, the protective effect of LPS is not antigen-specific and does not result from a general desensitization. These studies indicate that a single dose of LPS reduces the antigen-induced BC by reducing histamine release from lung mast cells, although a decreased formation of eicosanoids may contribute to the protective effect of LPS.

Animals↗
PubMed1990

Modulation of immune responses with monoclonal antibodies. I. Effects on regional lymph node morphology and on anti-hapten responses to haptenized monoclonal antibodies.

Repeated injections of monoclonal antibody (mAb) culture supernatants into rat footpads increased the weights of the draining lymph nodes. Immunostained freeze sections showed that injection of MRC OX2, a mAb reacting with rat follicular dendritic cells and MRC OX7 (anti-Thy-1.1), led to gross hypertrophy primarily of the follicular areas, whereas MRC OX6 (anti-rat major histocompatibility complex class II molecules) resulted in selective stimulation of the paracortex. These findings indicate that mAb, when conjugated to certain antigens, would modulate the immune response to these antigens. Consequently, the mAb were conjugated with fluorescein isothiocyanate (FITC) and the humoral response against the hapten measured. The primary anti-FITC antibody response was tenfold stronger than after stimulation with FITC conjugated to a conventional carrier such as ovalbumin, and had some characteristics of a secondary response: a fast increase of IgG level to very high titers and a long duration without further amplification at later antigen challenges.

Adjuvants, Immunologic↗
PubMed1996

Ligation of TAPA-1 (CD81) or major histocompatibility complex class II in co-cultures of human B and T lymphocytes enhances interleukin-4 synthesis by antigen-specific CD4+ T cells.

We have previously shown that CD4+ T cells from allergic individuals are predisposed to producing interleukin (IL)-4 in response to allergens. IL-4 production could be modulated by antigen concentration as well as by the type of antigen-presenting cells (APC), with B lymphocytes inducing greater quantities of IL-4 than monocytes. Using this system we examined IL-4 synthesis after culture of CD4+ T cells with B cells, monocytes, or both, as APC in the presence of allergen and a monoclonal antibody against CD81 (TAPA-1), a member of the TM4 superfamily of proteins that regulates activation, proliferation and trafficking of B cells. Addition of anti-CD81 mAb during culture enhanced IL-4 synthesis by 2- to 70-fold over that using an isotype-matched control mAb. Furthermore, anti-CD81 mAb enhanced IL-4 synthesis in CD4+ T cells only when CD4+ T cells were cultured with B cells but not monocytes as APC, indicating that anti-CD81 mAb affected IL-4 synthesis in T cells via interactions with B cells. However, pretreatment of either population separately with anti-CD81 mAb prior to culture had no effect on subsequent IL-4 synthesis, suggesting a requirement for temporal or cooperative interactions between T and B lymphocytes. In addition, anti-CD81 mAb enhanced IL-4 production but reduced CD4+ T cell antigen-specific proliferation, demonstrating that IL-4 production and proliferation by CD4+ T cells were inversely related. Finally, mAb to major histocompatibility complex class II but not to anti-CD19 also enhanced IL-4 synthesis when B lymphocytes were used as APC. In all instances, enhancement of CD4+ IL-4 synthesis correlated with the presence of large cell aggregates in T-B lymphocyte cocultures. These results indicate that the capacity of B cells to induce IL-4 can be significantly enhanced by ligation of particular molecules on their surface and should aid in the design of treatments for diseases in which modulation of the cytokine profile would be beneficial.

Antibodies, Monoclonal↗
PubMed1992

Possible mechanisms of immune modulation in chronic dermatophytoses: an in vitro study.

It has been suggested that patients with chronic superficial Trichophyton rubrum infection have defective cellular immunity to dermatophyte antigens. This may be due to a selective anergy to dermatophyte antigens or reflect the activity of dermatophyte-derived lymphocyte inhibitory factors. To explore these possibilities, we assessed lymphocyte transformation to a variety of recall antigens, including a cytoplasmic and exoantigen preparation of Trichophyton rubrum in 15 patients with chronic dermatophyte infection and 15 age- and sex-matched positive controls. In a duplicate set of experiments, autologous serum was replaced by heat-inactivated fetal calf serum. In addition, the direct effect of Trichophyton rubrum extracts on lymphoproliferation was assessed in vitro. Comparable lymphocyte transformation to each recall antigen was observed in patients and controls. Moreover, we found no evidence for a circulating dermatophyte-derived lymphocyte inhibitory factor in sera from patients with chronic superficial infection. A direct inhibitory effect of Trichophyton rubrum on lymphocyte proliferation to recall antigens was observed, however, at protein concentrations of > 10 micrograms/ml (exoantigen preparation) and > 25 micrograms/ml (cytoplasmic preparation). This inhibitory effect was rapidly reversible, not associated with loss of cell viability and maximal when added within 24 h of antigen to cultured lymphocytes. Class II MHC antigen HLA-DR, a surface marker of T-cell activation, was observed on inhibited lymphocytes co-cultured with antigen, suggesting the primary target for the inhibitory effect in vitro is the lymphocyte rather than the antigen-presenting cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Role of heme oxygenase in pulmonary response to antigen challenge in sensitized rats in vivo.

Heme oxygenase (HO) protects against oxidant-mediated lung injury. However, it is uncertain whether changes in HO activity modulate antigen-induced airway inflammation. We studied the effects of pretreatment with either hemoglobin, a HO inducer, or tin protoporphyrin (SnPP)-9, a specific HO inhibitor, on increases in pulmonary insufflation pressure (PIP) and plasma extravasation induced by intravenously injected ovalbumin (OA) antigen in rats sensitized to OA in vivo with Evans blue dye as a marker. Pretreatment with hemoglobin (300 mg/kg) significantly increased (p<0.01) and that with SnPP-9 (50 micromol/kg) significantly decreased (p<0.01) HO activity of the lung, but they failed to alter OA antigen (300 microg/kg)-induced increases in PIP. In contrast, hemoglobin pretreatment significantly decreased (p<0.01) and SnPP-9 pretreatment significantly increased (p<0.05) the leakage of dye induced by OA antigen in the trachea, main bronchi, and segmental bronchi. OA antigen-induced increases in plasma extravasation were also inhibited by superoxide dismutase (12,000 U/kg). These findings suggest the oxygen radicals are involved in increases in plasma extravasation induced by antigen challenge and HO protects against antigen-induced airway inflammation.

Animals↗
PubMed1985

Class II antigen expression and gamma interferon modulation of monocytes and retinal pigment epithelial cells from patients with retinitis pigmentosa.

Monocytes from retinitis pigmentosa patients express diminished amounts of class II (HLA-DR) antigens in comparison to normal individuals, normal siblings of retinitis pigmentosa patients, glaucoma patients, and macular degeneration patients. This observation is correlated with a subnormal production of IFN-gamma, a potent regulator of class II antigen expression. When monocytes from retinitis pigmentosa patients are treated with IFN-gamma, the decreased expression of HLA-DR on the cell surface is restored to levels found on monocytes from normal individuals. HLA-DR antigens were detected on the surfaces of human retinal pigment epithelial cells grown in vitro and the expression of these antigens can be enhanced following IFN-gamma treatment. These data demonstrate an altered expression and regulation of class II, HLA-DR, antigens in a human eye disease. Since class II antigens and IFN-gamma are currently known to be necessary regulating proteins for efficient immune reactivity, these findings may indicate an immune disturbance in retinitis pigmentosa patients. Alternatively, this alteration may have nonimmune implications. For example, these studies may demonstrate an imbalance in systemic regulatory control systems and hence raise the possibility that these or related regulatory proteins and cell surface receptors may be instrumental in maintaining retinal integrity.

Cells, Cultured↗
PubMed1998

5' processing of tRNA precursors can Be modulated by the human La antigen phosphoprotein.

Eukaryotic precursor (pre)-tRNAs are processed at both ends prior to maturation. Pre-tRNAs and other nascent transcripts synthesized by RNA polymerase III are bound at their 3' ends at the sequence motif UUUOH [3' oligo(U)] by the La antigen, a conserved phosphoprotein whose role in RNA processing has been associated previously with 3'-end maturation only. We show that in addition to its role in tRNA 3'-end maturation, human La protein can also modulate 5' processing of pre-tRNAs. Both the La antigen's N-terminal RNA-binding domain and its C-terminal basic region are required for attenuation of pre-tRNA 5' processing. RNA binding and nuclease protection assays with a variety of pre-tRNA substrates and mutant La proteins indicate that 5' protection is a highly selective activity of La. This activity is dependent on 3' oligo(U) in the pre-tRNA for interaction with the N-terminal RNA binding domain of La and interaction of the C-terminal basic region of La with the 5' triphosphate end of nascent pre-tRNA. Phosphorylation of La is known to occur on serine 366, adjacent to the C-terminal basic region. We show that this modification interferes with the La antigen's ability to protect pre-tRNAiMet from 5' processing either by HeLa extract or purified RNase P but that it does not affect interaction with the 3' end of pre-tRNA. These findings provide the first evidence to indicate that tRNA 5'-end maturation may be regulated in eukaryotes. Implications of triphosphate recognition is discussed as is a role for La phosphoprotein in controlling transcriptional and posttranscriptional events in the biogenesis of polymerase III transcripts.

Adenosine Triphosphatases↗
PubMed1984

Pure interferon gamma enhances class II HLA antigens on human monocyte cell lines.

Human recombinant interferon gamma (IFN-gamma) with a chemical purity of over 90% was shown to enhance membrane expression of HLA-DR antigens on cells from 3 human myelomonocytic lines (HL-60, U-937 and THP-1). Immunofluorescence techniques using a series of anti-HLA-DR monoclonal antibodies showed that the low, although variable, levels of DR-positive cells were clearly enhanced as soon as 24 h after incubation with IFN-gamma. Only IFN-gamma was able to exert this effect, since incubation with high concentrations of IFN-alpha or -beta did not induce any significant modification of the percentage of HLA-DR-positive cells. In contrast, doses of IFN-gamma as low as 2 units were effective, indicating a highly preferential, apparently selective effect of IFN-gamma for enhancement of HLA-DR expression. Private class II antigen expression was also enhanced by IFN-gamma on the U-937 cell line. Through its enhancing effect on class II public and private HLA antigens on the membrane of human monocytes, the IFN-gamma lymphokine may have a critical role in the modulation of antigen presentation by monocytes and on the regulation of HLA-DR-restricted cell cooperation.

Antibodies, Monoclonal↗
PubMed1992

Heterogeneity of immunoglobulin-associated molecules on human B cells identified by monoclonal antibodies.

Two covalently linked transmembrane molecules, encoded in mice by the mb-1 and B29 genes, have been defined as integral components of the antibody receptor units expressed on B cells. We have produced monoclonal antibodies against an exposed extracellular epitope on the putative human equivalent of the mouse B29 product. These antibodies, CB3-1 and -2, were used to show that cytoplasmic expression of this molecule begins in human pro-B cells (terminal deoxynucleotidyltransferase-positive, mu chain-negative), whereas surface expression coincides strictly with surface immunoglobulin expression of all isotypes. Immunochemical analysis of the human immunoglobulin-associated molecules revealed greater molecular heterogeneity than has been noted for the murine analogues. This molecular heterogeneity of immunoglobulin-associated molecules varied as a function of differentiation stage and the immunoglobulin isotypes expressed by B-lineage cells. Our data support the hypothesis that biochemical heterogeneity of the surface immunoglobulin-associated molecules may contribute to the variability in biological effects of antigen receptor crosslinkage on B cells of different maturational stages. Because the CB3 antibodies are capable of down-modulating the antigen receptors on all B cells, they may prove therapeutically useful as universal B-cell suppressants.

Antibodies, Monoclonal↗
PubMed1990

An SV40 large T antigen binding site in the cellular genome is part of a cis-acting transcriptional element.

A genomic mouse DNA fragment (Q300), containing a high affinity binding site for SV40 large T antigen, serves as a cis-acting transcriptional element in in vivo and in in vitro studies. We have performed experiments to investigate whether bound T antigen could modulate the promoter-enhancer activity of the Q300 element. In vivo studies showed a negative effect of T antigen on the Q300 driven expression of the chloramphenicol acetyl transferase reporter gene. Band shift and DNAase I protection experiments demonstrated that T antigen and a nuclear protein, probably a CCAAT-binding factor, can simultaneously bind to closely adjacent sites on the Q300 DNA. Transcription studies in vitro showed that bound T antigen suppresses the transcriptional enhancer effect of the Q300 element. We interpret the results of these model studies to indicate that T antigen, bound to DNA, is able to affect the function of a cellular cis-acting transcriptional element. Bound T antigen may influence the activity of a cellular transcription factor at a closely adjacent DNA site.

Animals↗
PubMed2006

Modulation of DRAK2 autophosphorylation by antigen receptor signaling in primary lymphocytes.

Death-associated protein-related apoptotic kinase-2 (DRAK2), a member of the death-associated protein-like family of serine/threonine kinases, is highly expressed in lymphoid organs and is a negative regulator of T cell activation. To investigate the regulation of DRAK2 activity in primary lymphocytes, we employed mass spectrometry to identify sites of autophosphorylation on DRAK2. These studies have revealed a key site of autophosphorylation on serine 12. Using a phospho-specific antibody to detect Ser(12) phosphorylation, we found that autophosphorylation is induced by antigen receptor stimulation in T and B cells. In Jurkat T cells, resting B cells and thymocytes, DRAK2 was hypophosphorylated on Ser(12) but rapidly phosphorylated with antigen receptor ligation. This increase in phosphorylation was dependent on intracellular calcium mobilization, because BAPTA-AM blocked DRAK2 kinase activity, whereas the SERCA inhibitor thapsigargin promoted Ser(12) phosphorylation. Our results show that DRAK2 kinase activity is regulated in a calcium-dependent manner and that Ser(12) phosphorylation is necessary for optimal suppression of T cell activation by this kinase, suggesting a potential feedback loop may act to modulate the activity of this kinase following antigen receptor signaling.

Animals↗
PubMed1993

"Neutral allografts"--lack of allogeneic stimulation by cultured human cells expressing MHC class I and class II antigens.

Cultured human dermal fibroblasts, smooth muscle cells, epidermal cells and endothelial cells were tested for immunogenicity in an in vitro allostimulation assay. Gamma interferon was used to induce MHC class II expression, since these cells constitutively express class I but not class II antigens. In contrast to human dermal fibroblasts, smooth muscle cells and epidermal cells, endothelial cells, were able to stimulate a significant proliferative response in normal allogeneic lymphocytes. Since ICAM-1 was also expressed on these cells, this inability to initiate allostimulation was probably not due to the absence of adhesion molecules. Addition of exogenous cytokines such as IL-1, IL-2, and TNF did not restore T cell proliferation in the test system. Therefore the inability of dermal fibroblasts, smooth muscle cells, and epidermal cells to initiate significant allostimulation was also not due to lack of cytokine production. It appears that certain cells lack as-yet-undefined costimulatory factors required for their effective recognition as foreign. These results support the notion that cultured human fibroblasts, smooth muscle cells, and epidermal cells could serve as building blocks of engineered "neutral allografts" for use across MHC barriers.

Antigenic Modulation↗
PubMed1988

Transmembrane signalling by B-lymphocyte receptors.

The responses of B cells to specific antigens are modulated by secondary signals delivered by a variety of cell surface receptors. Besides surface immunoglobulins, these include class II MHC antigens, Fc and C3 receptors, in addition to those for various lymphokines. The current knowledge of the second messengers used by various receptors and their roles in B-cell activation are discussed here.

Animals↗