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PubMed1989

The influence of C3-coated homologous erythrocytes on pokeweed-mitogen-induced polyclonal differentiation of human B cells.

The present study was undertaken in order to test the hypothesis that homologous erythrocytes (E) coated in vivo with C3d could modulate the immunoglobulin (Ig) synthesis of human peripheral blood mononuclear cells (PBMC), stimulated with pokeweed mitogen (PWM) in vitro. E from healthy individuals were found to enhance markedly the Ig synthesis of PMBC cultures stimulated with suboptimal doses (0.01 microgram/ml) of PWM. E coated in vivo with increasing amounts of C3d (1.4-6.3 times the amounts on normal E), obtained from patients with systemic lupus erythematosus, failed to induce any significant increase in Ig synthesis of PBMC cultures stimulated with suboptimal PWM doses, compared with cultures co-stimulated in parallel with normal E. In contrast, an increase in IgM and IgG synthesis was observed in about 50% of PBMC cultures from different donors when stimulated with PWM in the presence of E coated with C3b in vivo (from a patient with congenital factor I deficiency), compared with the Ig synthesis in cultures co-stimulated in parallel with normal E. In contrast to the inability of C3d-coated E to modulate B-cell proliferation, the monoclonal anti-CR2 antibody OKB7 was found to be mitogenic for unstimulated peripheral B cells.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1992

Complement receptor type 2 mediates infection of the human CD4-negative Raji B-cell line with opsonized HIV.

Opsonization of the HTLV-RF and HTLV-IIIB strains of HIV-1 with normal human HIV seronegative serum under conditions that allow complement activation resulted in the productive infection of cells of the Raji B lymphoblastoid cell line. Under the same experimental conditions, no infection of Raji cells was observed with unopsonized virus. Infection of Raji cells with complement-opsonized HIV-1 was totally suppressed by preblocking the function of CR2 (the C3dg receptor, CD21) on the cells with a monoclonal anti-CR2 antibody cross-linked with rabbit F(ab')2 anti-mouse immunoglobulin antibodies. Infection of Raji cells occurred independently of CD4 since the cells lacked the expression of CD4 antigen and of CD4 transcripts. Thus, Raji cells may be infected with complement-opsonized HIV independently of CD4 and in the absence of antibodies. By mediating and/or enhancing HIV infection, complement and complement receptors contribute to extend the range of target cells to the virus and may increase infection in patients with a low viral load.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Evidence for the role of CR1 (CD35), in addition to CR2 (CD21), in facilitating infection of human T cells with opsonized HIV.

Complement activation by HIV results in the binding of C3 fragments to the gp160 complex and enhanced infection of C3 receptor-bearing target cells. We have studied complement-mediated enhancement of infection of the human CD4-positive T-cell line HPB-ALL which expresses the CR1 (CD35) and CR2 (CD21) receptors for C3. CR1 and CR2 are present on 15% and 40% of normal peripheral blood CD4-positive T lymphocytes respectively. Opsonization of the virus with complement resulted in a 3- to 10-fold enhancement of infection of HPB-ALL cells, as assessed by measuring the release of p24 antigen in culture supernatants throughout the culture period. Blockade of CR2 with cross-linked anti-CR2 monoclonal antibodies decreased infection to the level observed with unopsonized virus. Blocking CR1 reduced complement-mediated infection by 50-80%. Experiments using serum deficient in complement factor I demonstrated that CR1 mediates the interaction between opsonized virus and T cells in addition to its ability to serve as a cofactor for the cleavage of C3b into smaller fragments that interact with CR2. A requirement for CD4 in complement-mediated enhancement of infection was observed with HIV-1 Bru but not with HIV-1 RF. Thus, CR1 and CR2 contribute in an independent and complementary fashion to penetration of opsonized virus into complement receptor-expressing T cells. Involvement of CD4 in infection with opsonized virus depends on the viral strain.

CD4 Antigens↗
PubMed2006

Role of dendritic cells in Sjögren's syndrome.

Sjögren's syndrome (SS) is a chronic inflammatory and lymphoproliferative autoimmune disease of unknown aetiology. It is characterised by progressive mononuclear cell infiltration of the salivary and lacrimal glands and a decreased glandular secretion, resulting in dryness of the mouth and eyes (xerostomia and keratoconjunctivitis sicca, respectively). Dendritic cells (DC) are considered to be the most potent antigen-presenting cells. Because of their central role in initiating an immune response while maintaining tolerance, impaired function of these cells might lead to the break of peripheral tolerance and initiation of immune responses to self-antigens. This review will focus on the possible role of DC in SS.

Animals↗
PubMed1980

The blocking effect of antibodies against the products of the H-2 gene complex on lymphocyte complement (C3d) receptors. complement dependence and specificity.

Antisera against the products of the major histocompatibility system (MHS), produced by immunization between congenic mouse strains differing only at that segment of the 17th chromosome rosettes which bears the H-2gene complex, exert a reproducible blocking effect on formation of with EACm (C3d rosettes). In many instances this effect is probably due to specific antibodies reactive with the lymphocytes, as indicated by immunochemical and adsorption experiments. Purified antibodies from the C3H anti-C3H.B10 immune ascites failed to exert this blocking effect. The blocking capacity can be restored, however, by addition of fresh normal mouse, rabbit or fetal calf serum, but not by heat inactivated serum. These experiments show that the presently defined H-2K, H-2D and H-2L antigens as well as some Ia antigens are themselves not the C3d receptors. The blocking effects observed in the presence of complement are possibly due to the proximity of H-2 or Ia molecules and C3d receptors, or to a rearrangement of membrane components after reaction with anti-MHC anti-MHC antibodies and complement.

Animals↗
PubMed2004

Increased expression of the B-cell-regulatory molecule CD72 in primary Sjögren's syndrome.

To determine whether there is an intrinsic abnormality of B-cell signaling in primary Sjögren's syndrome (pSS), the expression of B-cell coreceptors was determined in patients with primary Sjögren's syndrome and healthy and disease controls. Peripheral blood mononuclear cells were labeled with monoclonal antibodies to CD21, CD22, or CD72, and then the pan B-cell marker CD19. The expression of these coreceptors on the total CD19(+) population was determined. There was a significant increased expression of CD72 on the B cells of pSS patients (MFI, 215 +/- 6) compared to normal controls (MFI, 141 +/- 6). The increased CD72 expression was disease specific for pSS, as it was not observed in systemic lupus erythematosus or rheumatoid arthritis. The effect of B-cell stimulation on coreceptor expression was determined by culturing cells with B-lymphocyte-activating factor (BAFF) and/or pokeweed mitogen (PWM) or without either. Following culture, CD72 expression was decreased in both pSS and normal controls, regardless of the presence of BAFF or PWM. The upregulation of CD72 in pSS might be a compensatory response to increased B-cell receptor stimulation or a primary abnormality leading to uncontrolled B-cell activation.

Aged↗
PubMed1998

Lymphocyte subsets in human tonsils: the effect of age and infection.

The aim of the present study was to determine the effect of repeated tonsillitis on the development of lymphocyte subsets in the tonsils and among peripheral blood lymphocytes (PBL) of children. Subsets of T- and B cells were analyzed in the tonsils and in PBL of patients undergoing tonsillectomy for idiopathic tonsillar hypertrophy, recurrent tonsillitis, or tonsillar hypertrophy and tonsillitis. The majority of the CD4+ cells in the tonsils displayed the CD45RO+ phenotype, while the majority of those in the PBL displayed the CD45RA+ phenotype. Likewise, the proportion of CD45RO+CD8+ cells was higher in the tonsils than among PBL. The proportion of CD4 cells expressing the CD45RO marker increased with age among PBL, but not in the tonsils. B cells, detected by their CD19, CD20, and CD21 markers, were three times more abundant in the tonsils than in the PBL. The proportion of CD38+ cells showed a negative correlation with age, both in the tonsils and among PBL. Among PBL a striking age-related reduction was seen in the proportion of CD19+, CD21+ and CD38+CD21+ B cells. In contrast, in the tonsils age-related changes could be detected only in the proportion of CD21+CD38+ cells. No difference among patients with various clinical diagnoses was detectable in any of the T- and B cell subsets in the tonsils and PBL. Thus, lymphocyte subsets evolve independently in the tonsils and peripheral blood, with the repeated antigenic challenge of tonsillar lymphocytes not influencing circulating memory cells.

ADP-ribosyl Cyclase↗
PubMed1986

Comparisons of pooled polyclonal rabbit anti-human C3d with four monoclonal mouse anti-human C3ds. II. Quantitation of RBC-bound C3d, and characterization of antiglobulin agglutination reactions against RBC from 27 patients with autoimmune hemolytic anemia.

Labelled polyclonal IgG anti-C3d and monoclonal IgM and IgG anti-C3d antibodies (MAs) were employed at increasing antibody excess to measure the number of C3d molecules on human red blood cells (RBC) coated by complement in vitro and in vivo. Values for the number of C3d sites per cell determined with polyclonal anti-C3d were at least 4-fold higher than when MAs were used. The results suggest that the molar combining ratio for polyclonal anti-C3d with a single RBC-bound C3d fragment is more likely greater than 4.0 than 1.0 as previously assumed. Antiglobulin agglutination studies compared polyclonal and monoclonal anti-C3d antibodies against C3d-coated RBC from 27 patients with autoimmune hemolytic anemia. All four MAs showed striking prozones, requiring their use over a 25-fold higher range of dilutions than polyclonal anti-C3d. Polyclonal anti-C3d produced stronger agglutination reactions than any of the IgG MAs. Only the IgM MA produced agglutination as strong as, or stronger than, polyclonal anti-C3d. While IgM MA always gave the strongest MA agglutination reactions, no consistent ranking of the three IgG MAs was observed. Agglutination was not enhanced when all IgG MAs were combined; addition of IgG MAs to IGM MA reduced the strength of agglutination seen with IgM alone, suggesting blocking of IgM binding by competing IgG anti-C3d.

Anemia, Hemolytic, Autoimmune↗
PubMed1994

Interdigitating cell sarcoma: a morphologic and immunologic study of lymph node lesions in four cases.

Interdigitating cell sarcoma is an extremely rare tumor. Its presentation and histologic appearance has varied among the reported cases. In this study, the authors investigated four cases of the hematolymphoid malignancy arising within lymph nodes, which were considered to be of interdigitating cell origin. All patients presented in the 6th to 8th decade of life with peripheral lymphadenopathy, and had a relatively indolent clinical course, without bone marrow or skin involvement. Carcinomas were observed as a second neoplasm in two of four patients. Distinctive morphologic features are proliferation of histiocyte-like cells with nuclear pleomorphism and occasionally multinucleated, paracortical distribution sparing of B-cell regions, fibrosis, sinus infiltration, and a prominent eosinophil/plasma cell infiltrates. The combination of light microscopic, fine structural, and immunohistochemical features suggested that these tumors derive from interdigitating cells; these tumor cells expressed CD68 (KP1), S-100 protein and HLA-DR, but lack CD21 (1F8), desmosomes and Birbeck granules. The diagnosis of interdigitating cell sarcoma should be considered on any pleomorphic tumor with the features described in this report.

Aged↗
PubMed1997

Follicular dendritic cell sarcoma complicated by hyaline-vascular type Castleman's disease in a schizophrenic patient.

Follicular dendritic cell (FDC) sarcoma is an exceedingly rare neoplasm of unknown pathogenesis. A case of FDC sarcoma complicated by the hyaline-vascular type Castleman's disease occurring in a schizophrenic male is presented. Swelling of the left cervical lymph node appeared in a 44-year-old male schizophrenic who had been medicated with major tranquilizers for 20 years. He had had a history of cervical lymphadenopathy 14 years before, for which a diagnosis of hyaline-vascular type Castleman's disease had been made. The present specimen, obtained from the same site, was an enlarged lymph node heavily infiltrated with oval to spindle-shaped atypical cells but was uninvolved at the periphery. The infiltrating cells showed nodular or sheet-like growth, occasionally taking fascicular or storiform patterns. Follicular involvement was also common. Peculiarly, various amounts of small lymphocytes were intermingled with the neoplastic cells. The atypical cells expressed two FDC-specific antigens, DRC-1 and Ki-M4 antigen, together with a few other markers that are shared by FDC, including CD21 and HLA-DR. These findings clearly show the tumor to be FDC sarcoma. In addition, a peculiar fibro-hyalinous change in the lymph follicle, which is compatible with hyaline-vascular type Castleman's disease, was noted at the periphery of the lymph node where neoplastic cells had not infiltrated. Surprisingly, similar hyaline-vascular changes were observed in the previous biopsy taken 14 years ago. Meanwhile, Kaposi's sarcoma-associated herpesvirus, which is often identified from generalized Castleman's disease, was not identified in the present case by polymerase chain reaction study. Thus, this case is unique in two aspects: (i) the overlap of FDC sarcoma with hyaline-vascular type follicular changes; and (ii) its occurrence in a schizophrenic patient.

Adult↗
PubMed2005

Epstein-Barr virus infection in sarcomatoid renal cell carcinoma tissues.

OBJECTIVE: To determine whether Epstein-Barr virus (EBV) infection is related to renal cell carcinoma (RCC) tissues. MATERIALS AND METHODS: We investigated EBV infection and its genotypes in 73 cases of different types of RCC and 18 of non-neoplastic kidney. EBV infection and its genotypes were determined by EBV-encoded RNAs in situ hybridization (EBER-ISH) and polymerase chain reactions for EBV-encoded nuclear antigen 1 (EBNA-1) and EBNA-3C. The immunophenotype and EBV status of the EBV-infected cells were examined by double-labelling of EBER-ISH and/or immunohistochemistry for lymphoid cell markers, EBV proteins, and CD21. RESULTS: EBER-ISH signals were detected in five of 73 RCC tissues (6.8%), but in none of 18 non-neoplastic kidneys. Interestingly, EBER-ISH was positive only in five of the 10 sarcomatoid RCCs, and of these, four also showed amplification of EBNA-1. EBV was located exclusively in the tumour-infiltrating B lymphocytes of sarcomatoid RCCs. The genotype of EBV was determined as type 1. A few EBV-infected B cells expressed BZLF1 (an EBV immediate-early gene product) while none expressed EBNA-2 or latent membrane protein 1. This indicates that the B cells are of EBV latency type I, often replicating EBV. EBV infection did not affect the survival rates of patients with sarcomatoid RCC (P = 0.635, Kaplan-Meier analysis, log-rank test). CONCLUSION: EBV is present only in tumour-infiltrating B lymphocytes of sarcomatoid RCCs. The present study suggests that sarcomatoid RCC modulates a function of EBV-specific T cells controlling EBV replication, or stimulates differentiation of memory B cells into plasma cells.

Adult↗
PubMed1984

p69,71 antigen complex detected by monoclonal antibody Leu 1 in the identification of particular stages of malignant B-cell differentiation.

Lymphomatous cell samples from 86 patients with B-cell neoplasia (34 chronic lymphocytic leukaemia, 8 hairy-cell leukaemia, 5 prolymphocytic leukaemia, 20 immunocytic lymphoma, 9 centrocytic lymphoma, 3 centroblastic/centrocytic lymphoma, 3 lymphoblastic lymphoma, 1 plasma cell leukaemia and 3 plasmacytoma) were studied using the monoclonal antibody Leu 1, detecting a p69,71 antigen complex present on nearly all thymocytes, most (greater than 85%) peripheral T-lymphocytes as well as some malignant B-cells. Furthermore, we compared the reactivity of Leu 1-positive B-cells with those exhibiting conventional surface markers such as mouse-erythrocyte-receptor, FcIgG-receptor, C3b- or C3d-receptor and surface immunoglobulins of the various heavy- and light-chain types. Our results demonstrate a correlation between the expression of p69,71 antigen complex and distinct phenotypes revealed by conventional markers and underline the value of Leu 1 monoclonal antibody in the differential diagnosis of human B-cell neoplasia.

Antibodies, Monoclonal↗
PubMed1984

In situ characterization of cell infiltrates in human dental periapical granulomas. 2. Demonstration of receptors for the complement components C3b and C3d.

The inflammatory cell infiltrates in human dental periapical granulomas were studied through the demonstration of receptors (R) for fragments C3b and C3d of the complement component C3, C3bR and C3dR were detected in cryostat sections by the closed chamber hemadsorption technique. Sheep erythrocytes sensitized with rabbit IgM antibody and coated with human C3B or C3d were used as indicator cells. Of the 62 granulomas studied, 23 showed strong or moderate C3bR activity, and weak C3dR activity was detected in 5 out of 25 specimens. The C3bR activity was abolished by treatment with 0.25 mM periodic acid, indicating that carbohydrate is a part of the C3bR. Using an antiserum to C3R as first layer in indirect immunofluorescence experiments, the C3R was localized to cell membranes. The low C3dR activity indicates that a minor part of the mononuclear cells in the human periapical granulomas were B lymphocytes.

Adult↗
PubMed1998

Preliminary evidence for an association of Epstein-Barr virus with pre-ulcerative oral lesions in patients with recurrent aphthous ulcers or Behçet's disease.

In this study we used the polymerase chain reaction (PCR), slot blot and Southern blot hybridization, direct sequencing and in situ hybridization (ISH) to show the possible presence of EBV-DNA in pre-ulcerative oral aphthous lesions of patients with recurrent aphthous ulcers (RAU) or Behçet's disease (BD). For this purpose, formalin-fixed biopsy specimens were obtained from 13 pre-ulcerative oral aphthous lesions of nine RAU and four BD patients. Five specimens of normal oral mucosa (NOM) from five normal control subjects and 10 specimens of oral erosive or ulcerative lesions from 10 patients with erosive lichen planus (ELP) were also included. EBV-DNA was detected by PCR in 5 of the 13 (38.5%) pre-ulcerative oral aphthous lesions, two from RAU patients and three from BD patients. However, no EBV-DNA was demonstrated in five NOM specimens from normal control subjects and in 10 specimens of oral lesions from ELP patients. EBV-DNA was also demonstrated in patients' peripheral blood lymphocytes and/or plasma, suggesting that the lymphocytes may be the reservoir of latent EBV infection and there is EBV shedding in the plasma. EBV-DNA was detected by ISH in only one PCR-positive case; the reaction product was found to deposit on the nuclei of some of the epithelial cells and lymphocytes. By immunohistochemistry, expression of Epstein-Barr nuclear antigen and EBV/C3d receptors was also noted in some of the epithelial cells and lymphocytes in this ISH-positive case. Therefore, we suggest that the epithelial cells of pre-ulcerative oral aphthous lesions may be infected by EBV through EBV-infected lymphocytes; also, the cytotoxic T lymphocyte-induced lysis of the EBV-infected epithelial cells, but not the virus-induced cytolysis, may be the main mechanism causing oral ulcer formation. Our data provide preliminary evidence for an association of EBV with pre-ulcerative oral aphthous lesions in RAU and BD patients.

Adolescent↗
PubMed2006

Influence of proinflammatory cytokines on Actinobacillus actinomycetemcomitans specific IgG responses.

OBJECTIVE: High levels of serum anti-Actinobacillus actinomycetemcomitans immunoglobulin G (IgG) correlate with reduced extent and severity of periodontal disease and the present study was undertaken to begin testing the hypothesis that proinflammatory cytokines are important in the induction of optimal anti-A. actinomycetemcomitans IgG responses. BACKGROUND: Studies with pokeweed mitogen indicate that interleukin-1alpha (IL-1alpha) and IL-1beta are necessary for optimal IgG1 and IgG2 production and that prostaglandin E(2) (PGE(2)) and interferon-gamma (IFN-gamma) selectively promote IgG2, which is a major component of the anti-A. actinomycetemcomitans response in vivo. The pokeweed mitogen results suggest that these proinflammatory cytokines would also be necessary for optimal production of IgG specific for A. actinomycetemcomitans. METHODS: Peripheral blood mononuclear cells from A. actinomycetemcomitans-seropositive subjects with localized aggressive periodontitis were stimulated with A. actinomycetemcomitans in immune complexes capable of binding follicular dendritic cells that participate in the induction of recall responses in vivo. Cultures were manipulated with anti-IL-1alpha, anti-IL-1beta, anti-IFN-gamma, anti-IL-12, anti-CD21, indomethacin, and PGE(2). Actinobacillus actinomycetemcomitans specific IgG production was monitored by enzyme-linked immunosorbent assay (ELISA). RESULTS: Addition of follicular dendritic cells to peripheral blood mononuclear cells cultures resulted in follicular dendritic cell-lymphocyte clusters and increased anti-A. actinomycetemcomitans IgG responses (3-40-fold increases) compared with controls lacking follicular dendritic cells. Anti-IL-1alpha, anti-IL-1beta, anti-IFN-gamma, anti-IL-12, anti-CD21 and indomethacin suppressed anti-A. actinomycetemcomitans IgG production by half or more. PGE(2) restored IgG responses suppressed by indomethacin. CONCLUSIONS: The cytokines IL-1alpha, IL-1beta, IFN-gamma, IL-12, and PGE(2) were all necessary for optimal production of human anti-A. actinomycetemcomitans and the need for proinflammatory cytokines including the T helper 1 (Th1) cytokines is consistent with a response with a significant IgG2 component.

Actinobacillus Infections↗
PubMed1997

Lactation stage-dependent changes of lymphocyte subpopulations in mammary secretions: inversion of CD4+/CD8+ T cell ratios at parturition.

PROBLEM: Determination of lactation stage-dependent changes in levels of lymphocyte subpopulations in milk. METHOD: Flow cytometric assay was used to identify and assay lymphocyte subpopulations in bovine milk at different stages of lactation. RESULTS: Lymphocyte subpopulations in mammary secretions of dairy cows change during the lactation cycle. In involuting glands (dry gland), approximately 80-90% of lymphocytes were CD2+ T cells. The proportion of CD2+ T cells, however, decreased to approximately 50% at the colostral stage an fluctuated between 50 to 60% in normal (mature) milk. Throughout the lactation stages, less than 5% were B cells as identified by the monoclonal antibodies against CD21 and MHC class II antigens. Subset analysis showed, however, that the proportion of CD5+ T cells decreased from 90% in involuting gland secretions to 75% in colostrum (peripartum stage), and to approximately 40-50% in the normal (mature) milk, CD4+ T cells constituted between 45 to 55% of lymphocytes in the dry gland secretion but decreased drastically at parturition and maintained at the level below 20% throughout normal lactation. In contrast, the proportion of CD8+ T cells in the dry gland secretion was low, between 30 to 40%, but increased steadily, in an inversely-related manner with that of CD4+ T cells, to approximately 40-50% at parturition and maintained at approximately 30-40% during the normal lactation stage thereafter. Two-color immunofluorescence study revealed further that practically all of the CD8+ cells in dry gland secretions were CD2+, and approximately 40% of them were CD5-. Throughout the lactation cycle, WC1+ gamma delta T cells comprised only 2 to 5% of lymphocytes in mammary secretions. CONCLUSIONS: T lymphocyte subpopulations change dynamically during stages of the lactation cycle. The selective migration of T lymphocyte subpopulations to and from the mammary gland, and their functional roles in the immune competence and regulation of the dam and sucklings remain to be elucidated.

Animals↗
PubMed1989

Immunophenotype analysis of B-CLL lymphoma and immunocytoma.

The differential diagnosis between lymphocytic lymphoma of the B-CLL type and immunocytoma (IC) can be difficult when it is based only upon morphological criteria. With the aim of improving the distinction between these subgroups, frozen sections of lymph nodes or other biopsied tissues from 14 cases of B-CLL and 16 cases of IC were investigated according to immunophenotype. A panel of 13 B cell-associated and 2 T cell-associated monoclonal antibodies was used. All but one of the B-CLL cases were FMC7-, while 14/16 IC cases were FMC7+ (p less than 0.001). The two negative IC cases were both of the lymphoplasmacytic type, claimed to be "more differentiated" than the lymphoplasmacytoid type. We suggest that the cells in these cases are mature enough to have lost their FMC7 positivity, similar to plasma cells. There was also a statistically significant (p less than 0.01) difference, although not as pronounced, for the anti-CD38 antibody (Leu-17, B-CLL: 3/14, IC: 10/16 positive). No significant difference in expression of determinants was found for any of the other antibodies.

ADP-ribosyl Cyclase↗