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Biomedical subjects

B Pernis

Publications and source records attributed to B Pernis.

At least 55 records · Page 3Linked to original sources
PubMed1985

Physiology of IgD. V. Enhancement of antibody responses in vivo by allo anti-IgD is due primarily to an indirect effect on B cells.

Although responses of BALB/c mice to TNP-Ficoll or TNP-Brucella abortus are usually decreased by injection of allo anti-IgD (anti-Igh-5a) given 1 day before antigen, increased responses are obtained if a lymphokine mixture (SN) containing IL 2 is also injected. Simultaneous injection of anti-IgD and SN 4 days after priming with TNP-KLH induces an increase in antibody production similar to that induced by a second antigen injection. Injected together with a second injection of TNP-KLH at that time, anti-IgD and SN cause a synergistic enhancement of the secondary response. In allotype heterozygous (BALB/c X SJL)F1 mice injected with anti-IgD directed against one allotype, this enhancement of the secondary response is seen predominantly in the alternate allotype, because the IgG response of linked allotype specificity is slightly suppressed by the anti-IgD alone and is less enhanced than the alternate allotype by anti-IgD plus SN. Cells from unprimed heterozygous mice, incubated with anti-Igh-5a in vitro and transferred, together with antigen, to TNP-KLH-primed recipients, cause a much greater enhancement of the IgG responses of the Igb than of the Iga allotype in recipients. If, however, SN is also injected into the recipients, the anti-TNP response of both IgG allotypes is greatly enhanced.

Animals↗
PubMed1984

Acidification of internalized class I major histocompatibility complex antigen by T lymphoblasts.

It has previously been shown that activated murine T lymphocytes express intracellular vesicles containing the class I major histocompatibility complex (MHC) antigen H-2K. Evidence has also been provided that such vesicles may be part of a cellular pathway of spontaneous H-2K antigen internalization and recycling, which is specific to T-lymphoid cells. Dual fluorescence flow cytometry has now been used to establish that H-2K antigen is acidified upon internalization in concanavalin A-stimulated but not lipopolysaccharide-stimulated murine splenocytes, thus providing further support that in T lymphoblasts this class I MHC antigen may travel intracellular routes similar to those reported for other cell surface receptors.

Animals↗
PubMed1984

Physiology of IgD. IV. Enhancement of antibody production in mice bearing IgD-secreting plasmacytomas.

Immune responses to trinitrophenylated hemocyanin (TNP-KLH), Ficoll (TNP-Ficoll), and Brucella abortus (TNP-BA) were examined in BALB/c mice bearing subcutaneous transplants of TEPC-1017 and TEPC-1033, the two known IgD-secreting BALB/c plasmacytomas. Both primary and secondary 19S and 7S splenic plaque-forming cell (PFC) responses in spleen to intravenously injected TNP-KLH were enhanced three to fivefold. Primary responses to TNP-Ficoll were 1.5-2 times higher than in control mice (particularly the 7S PFC response). Primary responses to TNP-BA were enhanced by TEPC-1017 but suppressed by TEPC-1033, while secondary responses to TNP-BA were enhanced three to sevenfold by both tumors. Intraperitoneal injections of ascites fluid from mice bearing TEPC-1017 or TEPC-1033, or of IgD isolated from such ascites fluid, caused a similar enhancement of the primary response to TNP-KLH, as did the tumor itself, particularly when injected approximately 1 wk before antigen injection. IgD-containing ascites fluid had no effect on the response of athymic (nu/nu) BALB/c mice to TNP-KLH. These findings suggest the existence of an IgD-responsive immunoregulatory T cell.

Animals↗
PubMed1984

Spontaneous internalization of Class I major histocompatibility complex molecules in T lymphoid cells.

A low proportion of T lymphocytes in normal mouse spleen contains small intracytoplasmic vesicles showing Class I MHC molecules. After stimulation in vitro in a mixed lymphocyte reaction or by addition of Con A, the proportion of T cells with such intracytoplasmic vesicles increases progressively and becomes the majority. Labeling with fluorochrome-conjugated antibodies has shown that the vesicles are formed by internalization of molecules from the plasma membrane. The process is spontaneous and does not require cross-linking by antibodies or other ligands; it is selective inasmuch as other molecules (Thy-1 and T200 antigens) are not included and it is specific since it is not performed by other cells such as B lymphoid cells or fibroblasts. On the whole the process shows similarities with the internalization and recycling of other receptors, such as the receptors for different macromolecules of metabolic or informational significance, as seen in other cells. On the other hand, the specificity of Class I MHC mobilization in T lymphoid cells suggest a role for this process which is related to the immune function of these molecules.

Animals↗
PubMed1984

Physiology of IgD. III. Effect of treatment with anti-IgD from birth on the magnitude and isotype distribution of the immune response in the spleen.

Continued treatment with monoclonal anti-IgD (Ig-5a) from birth in BALB/c mice causes a markedly increased responsiveness to i.v. injected dinitrophenylated ovalbumin (DNP-OVA) with Bordetella pertussis at the age of 8 weeks. The 19S plaque-forming cell (PFC)/spleen response is particularly enhanced, 6-8-fold, but all the other isotypes also show increases of 2-6-fold, including IgA and IgE. Both primary and secondary PFC responses and serum antibody titers are enhanced. After transfer of spleen cells from anti-Ig-treated mice to irradiated recipients the IgM/IgG ratio becomes similar to that of controls. In contrast, the response of anti-IgD-treated mice to i.p. immunization with either 0.2 or 100 micrograms DNP-OVA plus alum is reduced by approximately 80% for each Ig isotype except IgM and remains low upon transfer of spleen cells to recipients. It is concluded that the paucity of B cells in peripheral lymph nodes of the anti-IgD-treated mice causes the low responsiveness to i.p. immunization, but that the IgD- B cells in the spleen are quite able to respond and are, in fact, more responsive than IgD+ B cells. This increased responsiveness, together with the higher IgM/IgG ratios for all Ig isotypes and an otherwise similar order of isotype distribution (gamma 1 greater than gamma 2b greater than gamma 2a = epsilon greater than or equal to alpha) as in controls, suggests that a hyperresponsive, but less mature IgD- B cell population is selectively produced in the spleens of mice treated with anti-IgD from birth.

Animals↗
PubMed1984

Murine streptozotocin diabetes: influences of the major histocompatibility complex, genetic background and blood transfusion.

Major histocompatibility complex-linked immune response genes are thought to influence susceptibility to induction of both human insulin-dependent diabetes and murine streptozotocin-induced diabetes. To clarify this relationship, we administered streptozotocin intravenously in two doses (120 and 240 mg/kg body weight) on days 0 and 14, and monitored blood glucose until day 100 in young adult male mice of differing background genome and/or H-2 complex. In addition, we examined the effect of allogeneic whole blood transfusion on subsequent susceptibility to diabetes. B10 recombinant mice possessing the k allele at the centromeric H-2-K and I-A loci were most susceptible to diabetes induction. Variation in susceptibility of different inbred strains with the same major histocompatibility complex genotype suggested a rôle for non-major histocompatibility complex genes. Blood transfusion delayed the onset, but did not significantly reduce the incidence of, delayed hyperglycaemia. We conclude that, in this murine model, multiple genes within the outside the major histocompatibility complex influence multiple-dose streptozotocin-diabetes susceptibility, and that prior blood transfusion may modulate diabetes induction.

Animals↗
PubMed1984

Idiotype expression in rheumatoid synovial plasma cells.

The majority of the polyclonal plasma cells identified in the synovial tissues of rheumatoid arthritis patients contain immunoglobulins that express a common idiotype related to that of the monoclonal cryoglobulins of the Wa group (RCRI). In these same tissues, there are twice as many plasma cells which are marked by a common idiotype yet do not show binding of aggregated IgG. These plasma cells are members of an idiotypically parallel set relative to those which produce rheumatoid factor. Direct comparison of rabbit polyclonal RCRI+ plasma cells with murine monoclonal RCRI+ plasma cells using two color fluorescent counterstains shows that the epitope recognized by the monoclonal anti-RCRI exists among a set of epitopes present in the RCRI. Since all the monoclonal RCRI+ plasma cells are not also positive with the polyclonal anti-RCRI antisera, the epitope characterized by the monoclonal antibody Glo 86.3 is not included among the set of epitopes the polyclonal antiserum identifies. A suitably absorbed anti-idiotypic polyclonal antiserum is superior to monoclonal antibodies for the purpose of detection of molecules (and cells) that are part of a polyclonal reaction involved in a given immune response.

Antibodies, Monoclonal↗
PubMed1984

Expansion of idiotype positive B cells in maternally idiotype suppressed mice.

The membrane expression of the J558 idiotype on B and T lymphocytes was studied in (A/J x BALB/c)F1 and (CAL.20 x BALB/c)F1 mice who were maternally suppressed for this idiotype. Animals suppressed in this fashion exhibit a chronic inability to synthesize J558 Id bearing antibodies in response to an antigenic challenge by alpha 1,3 linked dextran. However, by immunofluorescence, we observed that these maternally suppressed animals actually exhibited a considerable increase of B lymphocytes, which bear endogenously synthesized membrane immunoglobulin expressing the J558-IdI. Furthermore, a subset of T cells emerges that we have previously described as Lyt2.2+ cells exhibiting the J558-IdI determinant, which are capable of transferring the suppression to naïve recipients [1]. The goal of the experiments described in this communication was to thoroughly characterize those B cell clones that are expanded during idiotype suppression. Therefore, we immortalized these J558 Id+ B cells from idiotype suppressed mice as hybridomas. Four hybridomas secreting monoclonal antibodies bearing the J558 IdI but devoid of any specificity for alpha 1,3 linked dextran were obtained. It was established that these monoclonal antibodies bear the J558-Id by two criteria; namely, their direct binding to a panel of monoclonal anti-J558 IdI and a single anti-J558 IdX antibody, as well as by blocking the interaction of J558 with these antibodies. Notable was the fact that they all bore kappa light chains, even though in anti-dextran antibodies the expression of the lambda light chain is required for the expression of this idiotype. These results reaffirm the notion that idiotypic determinants are three dimensional structures which can be reconstructed by a variety of heavy and light chain sequences. Furthermore, an idiotope used in the regulation of an immune response (as our data implicate the J558 IdI is) is borne by antibodies displaying diverse specificities, which are coordinately regulated through this common idiotope.

Animals↗
PubMed1983

Internalized membrane immunoglobulin meets intracytoplasmic DR antigen in human B lymphoblastoid cells.

The important role of type II antigens of the major histocompatibility complex (Ia and DR) in the antigen presentation and in the antigen-specific cooperation between T and B cells is by now firmly established. Human B lymphoblastoid lines MWE and BL were stained with different fluoresceinated anti-DR antibodies. Not only surface but intracytoplasmic DR structures were brightly stained. The intracellular stain accumulated in a cluster close to the nucleus. Different specificity controls were performed. MWE and BL cells quickly internalize membrane IgM if cross-linked by corresponding antibodies. The intracellular location of the vesicles containing these complexes showed substantial coincidence with DR-positive structures in the paranuclear location. It is speculated that IgM-ligand complexes meet internal DR molecules and are both reexpressed on the plasma membrane to be recognized by primed T cells.

Antibodies, Monoclonal↗
PubMed1983

Anti-immunoglobulins and their idiotypes: are they part of the immune network?

The anti-gamma globulins represent a very heterogeneous group of proteins with widely different specificities that might be considered a portion of the immune network. The hypothesis is presented that at least some of these proteins have other specificities, with the anti-gamma globulin reactivity being a secondary property. Anti-idiotypic antibodies are possible candidates. This is based on the low binding affinity for gamma globulin of many of these proteins and the results of CRI and sequence studies. All the proteins of the major CRI group have VKIIIb light chains, and these have a dominant but not total influence on this CRI. This has been evident from studies with rabbit antibodies and recently also with monoclonal hybridoma antibodies. Sequence studies have also demonstrated the similarity in light chains that, however, are not greater than with other VKIIIb chains; the heavy chains show little similarity except possibly in the J segment. The possibility is discussed that antibodies with secondary anti-gamma globulin binding properties might have selective advantages.

Animals↗
PubMed1983

Idiotypes on B lymphocytes: association with immunoglobulins.

Several idiotypic (Id) specificities have been identified by immunofluorescence on the membranes of B cells in the spleens of nonimmune mice. These determinants are displayed at frequencies varying from 0.22 to 1.83% of B cells and are entirely immunoglobulin (Ig) in nature. No Id determinants were observed on the membranes of four Slg- Abelson virus-transformed pre-B cell lines that are sensitive to LPS. Under our experimental conditions, we did not observe a significant increase in 3H-thymidine incorporation subsequent to the in vitro incubation of splenic lymphocytes from normal mice with various amounts of anti-Id antibodies specific for several cross-reactive (IdX) or individual Id. Similarly, in utero exposure to anti-Id antibodies against myeloma proteins specific for T-independent antigens displaying B cell mitogenic properties did not alter the proliferation of lymphocytes induced by these mitogens. In contrast, exposure to anti-Id antibodies in vitro as well as in utero had a profound and specific effect on the corresponding antibody responses and maturation of small lymphocytes into plasma cells. When normal B cells were cultured with the B cell mitogen LPS in the presence of anti-Id antibodies directed against the J558IdX, specific suppression of the maturation of IdX+ plasma cells was observed. In mice exposed to maternal anti-Id in utero, we observed a severe inability to mount an immune response to any compound that elicited antibody molecules bearing the Id that was complementary to the maternal anti-Id. These same maternally Id-suppressed mice, however, gave a normal response when the same compound was presented as a mitogen. Our results reinforce the concept that Id on membranes of B lymphocytes are associated only with Ig receptors and do not support the possibility of mitogen-like poly-clonal stimulatory properties of anti-Id antibodies.

Animals↗
PubMed1982

The role of macrophages and immunocytes in the pathogenesis of pulmonary diseases due to mineral dusts.

There is considerable evidence of generalized stimulation of the immune system in pulmonary dust diseases. This stimulation involves both the T- and the B-arms of the immune system. A reasonable explanation of this immune stimulation resides in an effect of the mineral dusts on the macrophages. This effect is likely to be mediated by the production of interleukin-1. Since the same substance also stimulates fibroblasts, a unified view of the pathogenesis of pulmonary dust diseases is now possible.

Dust↗
PubMed1982

Physiology of Igd. II. Lack of humoral immune responsiveness in lymph nodes of mice treated with anti-IgD from birth.

Previous studies have shown that anti-IgD-suppressed mice give normal primary and secondary splenic plaque-forming cell responses following i.v. challenge, although mice suppressed by the injection of anti-IgD from birth lack IgD-bearing cells in all lymphoid tissue examined. The present studies show that, in contrast, secondary immune responses in regional lymph nodes of such mice, even after i.v. priming with trinitrophenylated B. abortus, respond to a challenge injection in the footpad up to only less than 10% of control levels. When compared with respect to B cell numbers transferred, primed spleen cells from control and anti-IgD-suppressed mice are about equally effective in producing adoptive secondary plaque-forming cell responses in the spleens of recipient mice. Lymph nodes in recipients of anti-IgD-suppressed primed spleen cells show much lower responses than do lymph nodes in recipients of control primed cells, both upon immediate and delayed challenge with antigen in the footpads. It is concluded that the immunodeficiency caused by suppression with anti-IgD is much more marked in peripheral lymph nodes than in the spleen. The possible relationship of these results to the migratory properties of IgD+ as compared to IgD-B cells is discussed.

Aging↗