scholarly journals Targeting CD20+ B-lymphocytes in inflammatory dilated cardiomyopathy with rituximab improves clinical course: a case series

2019 ◽  
Vol 3 (3) ◽  
Author(s):  
Carsten Tschöpe ◽  
Sophie Van Linthout ◽  
Frank Spillmann ◽  
Maximilian G Posch ◽  
Petra Reinke ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
B Cell ◽  
B Lymphocytes ◽  
B Lymphocyte ◽  
Case Series ◽  
Developed Countries ◽  
Cell System ◽  
Limited Information ◽  
Autoimmune Myocarditis ◽  
Cell Surface Molecule

Abstract Background  The aetiology of dilated cardiomyopathy (DCM) is highly heterogeneous including genetic and/or acquired (infective, toxic, immune, endocrine, and nutritional) factors. The major part of acquired DCM in developed countries is caused by either viral or autoimmune myocarditis. It is believed that the activation of the T-lymphocyte cell system is the major pathomechanism underlying autoimmune myocarditis and inflammatory DCM (DCMi). However, in the hearts of a subset of patients, a significant number of CD20+ B-lymphocytes can be detected too. Limited information exists on the role of B-cell-dependent mechanisms in the progression of DCMi. Particularly CD20+ B-lymphocytes, which can be targeted by anti-CD20+ B-lymphocytes antibodies or inhibitors, might contribute to the pathogenesis of myocardial damage beyond antibody production. Case summary  Here, we present a case series of six patients with subacute and chronic endomyocardial biopsy-proven CD20+ B-lymphocyte-associated DCMi, where symptomatic heart failure therapy, with or without combined immunosuppressive therapy with steroid-based treatment regime, was insufficient to improve cardiac function. Five patients improved clinically several weeks after a standard infusion protocol with rituximab, a chimeric monoclonal antibody against the pan-B-cell surface molecule CD20. Discussion  Our case series shows that CD20+ B-lymphocyte persistence can play a pathophysiologic role in a subset of DCMi patients and highlights the potential of targeting CD20+ B cells in patients with prominent CD20+ B-lymphocyte persistence.

Fetal liver pro-B and pre-B lymphocyte clones: expression of lymphoid-specific genes, surface markers, growth requirements, colonization of the bone marrow, and generation of B lymphocytes in vivo and in vitro

1992 ◽  
Vol 12 (2) ◽  
pp. 518-530
Author(s):  
R Palacios ◽  
J Samaridis
Keyword(s):  
B Cell ◽  
B Lymphocytes ◽  
Stromal Cells ◽  
B Lymphocyte ◽  
Germ Line ◽  
Fetal Liver ◽  
Rag 1 ◽  
B Cell Precursors

We describe here the development and characterization of the FLS4.1 stromal line derived from 15-day fetal liver of BALB/c embryos and defined culture conditions that efficiently support the cloning and long-term growth of nontransformed B-220+ 14-day fetal liver cells at two stages of B-cell development, namely, pro-B lymphocytes (immunoglobulin [Ig] genes in germ line configuration) and pre-B cells (JH-rearranged genes with both light-chain Ig genes in the germ line state). All B-cell precursor clones require recombinant interleukin-7 (rIL-7) and FLS4.1 stromal cells for continuous growth in culture, but pro-B lymphocyte clones can also proliferate in rIL-3. None proliferate in rIL-1, rIL-2, rIL-4, rIL-5, rIL-6, or leukemia inhibitory factor. FLS4.1 stromal cells synthesize mRNA for Steel factor but not for IL-1 to IL-7; all pro-B and pre-B clones express c-Kit, the receptor for Steel factor, and a c-Kit-specific antibody inhibits the enhanced proliferative response of fetal liver B-220+ B-cell precursors supported by FLS4.1 stromal cells and exogenous rIL-7 but does not affect that promoted by rIL-7 alone. Northern (RNA) blot analysis of the expression of the MB-1, lambda 5, Vpre-B, c mu, RAG-1, and RAG-2 genes in pro-B and pre-B clones show that transcription of the MB-1 gene precedes IgH gene rearrangement and RNA synthesis from c mu, RAG-1, RAG-2, lambda 5, and Vpre-B genes. All clones at the pre-B-cell stage synthesize mRNA for c mu, RAG-1, and RAG-2 genes; transcription of the lambda 5 and Vpre-B genes seems to start after D-to-JH rearrangement in B-cell precursors, indicating that the proteins encoded by either gene are not required for B-cell progenitors to undergo D-to-JH gene rearrangement. These findings mark transcription of the MB-1 gene as one of the earliest molecular events in commitment to develop along the B-lymphocyte pathway. Indeed, both pro-B and pre-B clones can generate in vitro and in vivo B lymphocytes but not T lymphocytes; moreover, these clones do not express the CD3-gamma T-cell-specific gene, nor do they have rearranged gamma, delta, or beta T-cell antigen receptor genes.

scholarly journals Replication history of B lymphocytes reveals homeostatic proliferation and extensive antigen-induced B cell expansion

2007 ◽  
Vol 204 (3) ◽  
pp. 645-655 ◽  
Author(s):  
Menno C. van Zelm ◽  
Tomasz Szczepański ◽  
Mirjam van der Burg ◽  
Jacques J.M. van Dongen
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Expansion ◽  
B Lymphocyte ◽  
Somatic Hypermutation ◽  
Homeostatic Proliferation ◽  
History Of ◽  
Lymphocyte Homeostasis

The contribution of proliferation to B lymphocyte homeostasis and antigen responses is largely unknown. We quantified the replication history of mouse and human B lymphocyte subsets by calculating the ratio between genomic coding joints and signal joints on kappa-deleting recombination excision circles (KREC) of the IGK-deleting rearrangement. This approach was validated with in vitro proliferation studies. We demonstrate that naive mature B lymphocytes, but not transitional B lymphocytes, undergo in vivo homeostatic proliferation in the absence of somatic mutations in the periphery. T cell–dependent B cell proliferation was substantially higher and showed higher frequencies of somatic hypermutation than T cell–independent responses, fitting with the robustness and high affinity of T cell–dependent antibody responses. More extensive proliferation and somatic hypermutation in antigen-experienced B lymphocytes from human adults compared to children indicated consecutive responses upon additional antigen exposures. Our combined observations unravel the contribution of proliferation to both B lymphocyte homeostasis and antigen-induced B cell expansion. We propose an important role for both processes in humoral immunity. These new insights will support the understanding of peripheral B cell regeneration after hematopoietic stem cell transplantation or B cell–directed antibody therapy, and the identification of defects in homeostatic or antigen-induced B cell proliferation in patients with common variable immunodeficiency or another antibody deficiency.

scholarly journals IVIg modulates BCR signaling through CD22 and promotes apoptosis in mature human B lymphocytes

Blood ◽  
2010 ◽  
Vol 116 (10) ◽  
pp. 1698-1704 ◽  
Author(s):  
Jean-François Séïté ◽  
Divi Cornec ◽  
Yves Renaudineau ◽  
Pierre Youinou ◽  
Rizgar A. Mageed ◽  
...  
Keyword(s):  
B Cell ◽  
B Lymphocytes ◽  
B Lymphocyte ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Time Dependent ◽  
G1 Phase ◽  
Dependent Manner ◽  
Bcr Signaling ◽  
Sustained Activation

Abstract Among various mechanisms for interactions with B cells, intravenous immunoglobulin (IVIg) may operate through the insertion of its Fc part into the Fc-γ receptor, or the binding of its sialic acid (SA)–bearing glycans to the negatively regulating CD22 lectin. It appeared that IVIg reduces B lymphocyte viability in a dose- and time-dependent manner. Furthermore, we show by confocal microscopy that SA-positive IgG, but not SA-negative IgG bind to CD22. This interaction reduces the strength of B-cell receptor–mediated signaling trough down-regulating tyrosine phosphorylation of Lyn and the B-cell linker proteins, and up-regulating phospholipase Cγ2 activation. This cascade resulted in a sustained activation of Erk 1/2 and arrest of the cell cycle at the G1 phase. These changes may be accounted for the efficacy of IVIg in autoimmune diseases.

scholarly journals B lymphocytes express and lose syndecan at specific stages of differentiation.

1989 ◽  
Vol 1 (1) ◽  
pp. 27-35 ◽  
Author(s):  
R D Sanderson ◽  
P Lalor ◽  
M Bernfield
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
B Lymphocyte ◽  
Plasma Cells ◽  
Receptor Expression ◽  
Cell Stage ◽  
Precursor B Cells

Lymphopoietic cells require interactions with bone marrow stroma for normal maturation and show changes in adhesion to matrix during their differentiation. Syndecan, a heparan sulfate-rich integral membrane proteoglycan, functions as a matrix receptor by binding cells to interstitial collagens, fibronectin, and thrombospondin. Therefore, we asked whether syndecan was present on the surface of lymphopoietic cells. In bone marrow, we find syndecan only on precursor B cells. Expression changes with pre-B cell maturation in the marrow and with B-lymphocyte differentiation to plasma cells in interstitial matrices. Syndecan on B cell precursors is more heterogeneous and slightly larger than on plasma cells. Syndecan 1) is lost immediately before maturation and release of B lymphocytes into the circulation, 2) is absent on circulating and peripheral B lymphocytes, and 3) is reexpressed upon their differentiation into immobilized plasma cells. Thus, syndecan is expressed only when and where B lymphocytes associate with extracellular matrix. These results indicate that B cells differentiating in vivo alter their matrix receptor expression and suggest a role for syndecan in B cell stage-specific adhesion.

Loss of Ubr1 Cooperatively Synergizes with HOX11 in B Cell Lymphomagenesis.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 215-215
Author(s):  
Edwin Chen ◽  
Suzana Rosic-Kablar ◽  
Lim S. Megan ◽  
Hough R. Margaret
Keyword(s):  
B Cell ◽  
B Lymphocytes ◽  
Insertional Mutagenesis ◽  
B Lymphocyte ◽  
B Cell Lymphoma ◽  
Cyclin B1 ◽  
Cell Cycle Checkpoint ◽  
Chromosome Loss ◽  
B Cell Lymphomas ◽  
Lymphocyte Cultures

Abstract The HOX11 homeobox gene was originally identified at the recurrent t(10;14)(q24;q11) translocation breakpoint, a chromosomal abnormality observed in 5–7% of T cell acute lymphoblastic leukemias (T-ALLs). Transgenic mice ectopically expressing HOX11 in the B cell compartment die in their second year of life due to the onset of mature B cell lymphomas. However, the long latency prior to the development of leukemia has led to the hypothesis that additional mutations are necessary prior to the onset of full-blown malignancy. To identify collaborating genetic loci responsible for HOX11-induced B cell lymphomagenesis, proviral insertional mutagenesis, using the mature B cell-specific retrovirus, the murine AIDS (mAIDS) virus, was used. In eight of ten animals, there was an acceleration of development of B cell lymphomas, manifested by the development of a mediastinal mass comprising predominantly of mature IgM+ IgD+ B cells. Histological analysis revealed expansion of splenic germinal centres and hyperplasia of adjacent lymph nodes, consistent with diffuse large B cell lymphoma. Using the provirus as a molecular tag, we identified Ubr1 as a frequent site of proviral insertion. Three mice exhibited an insertion into the 10th exon of the Ubr1 gene, with two animals exhibiting an identical insertion at nucleotide 1295 and another animal exhibiting an insertion at nucleotide 1251. Insertion into this genomic region was confirmed by Southern blotting demonstrating the presence of a rearranged Ubr1 allele, and by the ability to generate a PCR amplicon across the viral-genome junction. Western immunoblot analysis revealed down-regulated expression of the Ubr1 gene product subsequent to viral integration. Ubr1 is a member of the E3 ubiquitin ligase family and participates in the ubiquitin-dependent proteolytic pathway. Among its numerous targets, Ubr1 controls the timely degradation of cohesin subunits during mitosis. Consequently, Ubr1−/−S. cerevisiae are prone to chromosome loss due to chromosome malsegregation during anaphase. We sought to investigate possible similar effects in primary B lymphocyte cultures derived from HOX11Tg/Ubr1+/+ and HOX11Tg/Ubr1−/− mice, and to determine whether HOX11 overexpression in such a Ubr1-null background possesses any synergizing effects on the ploidy of these cells. Direct counting of chromosome numbers from chromosome spreads prepared from HOX11Tg/Ubr1−/− primary B lymphocytes cultured in vitro for 4–5 days revealed increased incidences of aneuploidy and chromosome loss relative to HOX11wt/Ubr1−/− controls (2n=39.51 vs. 2n=39.98). Similarly, micronucleus assays indicated increased presence of micronuclei in HOX11Tg/Ubr1−/− primary B lymphocyte cultures (5.2% vs 0.8%). Additionally, HOX11Tg B lymphocytes exhibit increased cyclin B1 expression and an ability to bypass G2-M arrest induced by the tyrosine kinase inhibitor, genistein. Therefore, the effect of HOX11 in exacerbating chromosome loss in these cultures may be associated with its ability to allow cells to bypass the G2-M cell cycle checkpoint, permitting the accrual of additional chromosome losses and cytogenic abnormalities en route to malignancy.

Expansion of Immature/Transitional B-Lymphocytes in Patients with Active Chronic Graft-Versus-Host Disease.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1065-1065
Author(s):  
Michal Kouba ◽  
Hildegard T. Greinix ◽  
David Pohlreich ◽  
Ulrike Körmöczi ◽  
Imke Lohman ◽  
...  
Keyword(s):  
B Cell ◽  
B Lymphocytes ◽  
Graft Versus Host Disease ◽  
Immune Reconstitution ◽  
B Lymphocyte ◽  
Development Project ◽  
Consensus Development ◽  
Graft Versus Host ◽  
Cell Subpopulations ◽  
Sampling Event

Abstract Background: Chronic graft-versus-host disease (cGVHD) is a major complication of allogeneic hematopoietic stem cell transplantation (HSCT) and an important cause of non-relapse mortality. The diagnosis of cGVHD depends mainly on clinical signs and histopathological confirmation. CGVHD is known to impair immune reconstitution. Recently, we observed that percentages of both non-class-switched (CD19+/IgD+/CD27+) and class-switched memory B-lymphocytes(CD19+/IgD−/CD27+) were significantly lower in patients with active cGVHD when compared to patients never experiencing cGVHD (p=0.003 and p= 0.001). The ratio of immature/memory B-lymphocytes (CD21−/CD27+) was significantly higher in patients with active cGVHD when compared to patients never experiencing cGVHD (p=0.0046). In the current study we investigated the influence of cGVHD on the pattern of immune reconstitution of B-cell subpopulations within the first years after HSCT. Methods: Ninety-nine patients (median age 42 years, range 17–62 years) were analyzed 3 months to 12 years after HSCT. The total of 212 sampling events included 141 samples obtained during active cGVHD and 71 samples from time points without cGVHD. Evidence of cGVHD in at least one organ as defined by the NIH Consensus Development Project was required to assign the sampling event into the active cGVHD group. The series included 10 patients (3 without and 7 developing cGVHD) assessed serially in 3 months’ intervals within the first years after HSCT. Peripheral blood leukocytes were analyzed by multiparameter flow cytometry after staining for CD19, staining for surface Ig and the B-lymphocyte memory marker CD27 as well as staining for CD21, which is absent on immature/transitional B-lymphocytes. The patients were scored for cGVHD activity according to the NIH Consensus Development Project criteria at every sampling event. Results: While the CD21−/CD27+ ratio as well as the percentage of immature/transitional B-lymphocytes decreased in the first years after HSCT in patients without cGVHD, these parameters remained significantly higher over the years in patients with active cGVHD (p=0.001). In logistic regression analysis a higher CD21−/CD27+ ratio and higher percentage of immature B-lymphocytes (CD21−) significantly correlated with active cGVHD. The odds ratio increased from 1.028 to 14.532 between the second and seventh year after HSCT. Until the end of the first year after HSCT serially sampled patients without cGVHD and the ones with cGVHD responding to immunosuppressive therapy presented a decrease of immature/transitional B-lymphocytes and increase of class-switched memory B cells whereas this pattern was disturbed in all serial patients with refractory cGVHD. Conclusions: Our study demonstrates that cGVHD is associated with an impairment of the reconstitution of the B-lymphocyte compartment leading to a long-lasting expansion of immature/transitional B-lymphocytes. Prospective studies with larger patient numbers analyzed serially are warranted for further assessment of the role of B-cell subpopulations in the pathogenesis of cGVHD and as potential biomarkers for cGVHD activity.

scholarly journals Human B-lymphocyte antigens expressed by lymphocytic and myelocytic leukemia cells. I. Detection by rabbit antisera.

1976 ◽  
Vol 144 (1) ◽  
pp. 167-178 ◽  
Author(s):  
R Billing ◽  
B Rafizadeh ◽  
I Drew ◽  
G Hartman ◽  
R Gale ◽  
...  
Keyword(s):  
B Cell ◽  
B Lymphocytes ◽  
Cell Lines ◽  
B Lymphocyte ◽  
Lymphocytic Leukemia ◽  
Immunofluorescent Staining ◽  
Leukemia Cells ◽  
Acute Myelocytic Leukemia ◽  
Normal Peripheral Blood ◽  
Myelocytic Leukemia

A previously uncharacterized human B-lymphocyte antigen has been detected by rabbit antisera raised to papain digests of spleen cell membranes. The unabsorbed sera reacted in both cytotoxicity and immunofluorescent tests with normal B lymphocytes and cultured B-cell lines but not with normal T lymphocytes or cultured T-cell lines. The cytotoxicity titers against B cells were as high as 1:32,000, whereas the same sera undiluted were negative against T cells. By immunofluorescent staining 6-14% of unfractionated normal lymphocytes and 48-85% of B-rich lymphocyte preparations were positive. Normal peripheral blood granulocytes, platelets, erythrocytes, and phytohemagglutinin blasts were negative. The antisera reacted with the same high titers against leukemia cells from approximately 70% of the patients with acute lymphocytic leukemia, acute myelocytic leukemia, chronic myelocytic leukemia, and seven of eight cases of chronic lymphocytic leukemia. From absorption studies it appeared that the same antigen was being expressed by leukemia cells and normal B lymphocytes. Using immunofluorescent staining the anti-B-cell antisera were able to detect positive leukemia cells in the bone marrow of patients with advanced leukemia and to monitor the elimination of these cells after chemotherapy. Soluble B-cell antigen was found in the serum of some leukemia and lymphoma patients do but not in normal serum.

scholarly journals B Lymphocyte Chemotaxis Regulated in Association with Microanatomic Localization, Differentiation State, and B Cell Receptor Engagement

1998 ◽  
Vol 187 (5) ◽  
pp. 753-762 ◽  
Author(s):  
Conrad C. Bleul ◽  
Joachim L. Schultze ◽  
Timothy A. Springer
Keyword(s):  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Messenger Rna ◽  
B Lymphocyte ◽  
Somatic Hypermutation ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Cxc Chemokine

Migration of mature B lymphocytes within secondary lymphoid organs and recirculation between these sites are thought to allow B cells to obtain T cell help, to undergo somatic hypermutation, to differentiate into effector cells, and to home to sites of antibody production. The mechanisms that direct migration of B lymphocytes are unknown, but there is evidence that G protein–coupled receptors, and possibly chemokine receptors, may be involved. Stromal cell– derived factor (SDF)-1α is a CXC chemokine previously characterized as an efficacious chemoattractant for T lymphocytes and monocytes in peripheral blood. Here we show with purified tonsillar B cells that SDF-1α also attracts naive and memory, but not germinal center (GC) B lymphocytes. Furthermore, GC B cells could be converted to respond to SDF-1α by in vitro differentiation into memory B lymphocytes. Conversely, the migratory response in naive and memory B cells was significantly reduced after B cell receptor engagement and CD40 signaling. The receptor for SDF-1, CXC chemokine receptor 4 (CXCR4), was found to be expressed on responsive as well as unresponsive B cell subsets, but was more rapidly downregulated on responsive cells by ligand. Finally, messenger RNA for SDF-1 was detected by in situ hybridization in a layer of cells surrounding the GC. These findings show that responsiveness to the chemoattractant SDF-1α is regulated during B lymphocyte activation, and correlates with positioning of B lymphocytes within a secondary lymphoid organ.

scholarly journals B Cells in Primary Membranous Nephropathy: Escape from Immune Tolerance and Implications for Patient Management

2021 ◽  
Vol 22 (24) ◽  
pp. 13560
Author(s):  
Benjamin Y. F. So ◽  
Desmond Y. H. Yap ◽  
Tak Mao Chan
Keyword(s):  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Membranous Nephropathy ◽  
Patient Management ◽  
B Lymphocyte ◽  
Somatic Hypermutation ◽  
Peripheral Tolerance ◽  
Cell Tolerance ◽  
B Cell Tolerance

Membranous nephropathy (MN) is an important cause of nephrotic syndrome and chronic kidney disease (CKD) in adults. The pathogenic significance of B cells in MN is increasingly recognized, especially following the discovery of various autoantibodies that target specific podocytic antigens and the promising treatment responses seen with B cell depleting therapies. The presence of autoreactive B cells and autoantibodies that bind to antigens on podocyte surfaces are characteristic features of MN, and are the result of breaches in central and peripheral tolerance of B lymphocytes. These perturbations in B cell tolerance include altered B lymphocyte subsets, dysregulation of genes that govern immunoglobulin production, aberrant somatic hypermutation and co-stimulatory signalling, abnormal expression of B cell-related cytokines, and increased B cell infiltrates and organized tertiary lymphoid structures within the kidneys. An understanding of the role of B cell tolerance and homeostasis may have important implications for patient management in MN, as conventional immunosuppressive treatments and novel B cell-targeted therapies show distinct effects on proliferation, differentiation and reconstitution in different B cell subsets. Circulating B lymphocytes and related cytokines may serve as potential biomarkers for treatment selection, monitoring of therapeutic response and prediction of disease relapse. These recent advances in the understanding of B cell tolerance in MN have provided greater insight into its immunopathogenesis and potential novel strategies for disease monitoring and treatment.

scholarly journals CELL INTERACTIONS BETWEEN HISTOINCOMPATIBLE T AND B LYMPHOCYTES

1973 ◽  
Vol 137 (6) ◽  
pp. 1405-1418 ◽  
Author(s):  
David H. Katz ◽  
Toshiyuki Hamaoka ◽  
Baruj Benacerraf
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cell ◽  
B Lymphocytes ◽  
B Lymphocyte ◽  
Cell Interaction ◽  
Antibody Responses ◽  
T And B Lymphocytes ◽  
Cooperative Interactions

Several experimental approaches, designed specifically to circumvent the possible contribution of a complicating "allogeneic effect," have been successfully used to answer the question of physiologic cooperative interactions between histoincompatible T and B lymphocytes in antibody responses to hapten-protein conjugates. This was accomplished for in vivo cell transfer studies by using an F1 hybrid host as the recipient of irradiated, carrier-primed T lymphocytes from one parent and 2,4-dinitrophenyl (DNP)-primed B lymphocytes from the opposite strain. Under these conditions, very good T-B cell cooperative interactions were observed to occur between T and B lymphocyte populations derived from syngeneic donors, whereas no cooperative response was obtained when T cells were derived from one parental strain and B cells from the other. Corroborative experiments were performed in a totally in vitro system in which DNP-primed B cells developed good secondary anti-DNP antibody responses in vitro to soluble DNP-keyhole limpet hemocyanin (KLH) when cultured in the presence of irradiated KLH-primed T cells derived from syngenic donors but not from allogeneic donors. The failure of histoincompatible T and B lymphocytes to effect physiologic cooperative interactions has important implications for our understanding of how such interactions normally occur. The possibility that these results reflect the existence of a "block" of some sort to cell-cell interaction by virtue of the presence of a foreign major histocompatibility antigen on the surface of either cell has been definitively ruled out in the present studies. These observations demonstrate that the gene(s) that conditions the capability for physiologic T-B cell cooperation must be shared in common by the respective cell types, and suggest, furthermore, that this gene (or genes) belongs to the major histocompatibility system of the mouse. These findings, together with other relevant phenomena described previously, have led us to postulate that there exists on the B lymphocyte surface an "acceptor" molecule either for the putative active T cell product or for the T cell itself. The important genetic considerations and the possible sequence of events surrounding the actual T-B cell interaction implied by these postulates are discussed in detail.

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