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At least 19 recordsLinked to original sources
PubMed1991

[Secondary deficiencies of humoral immunity].

Humoral immunity involves molecules in solution in biological fluids including effectors of non specific immunity (e.g. complement, cytokines) and specific immunity (antibodies) as well. Acquired humoral immunodeficiences are often multifactorial in origin and associated with defects of cell-mediated immunity. The most common etiologies are those of iatrogenic immunodeficiencies: surgery (especially splenectomy), radiotherapy, chemotherapy of leukemia and cancer, immunosuppressive treatments in organ transplanted patients. Protein-caloric malnutrition also induces cellular and humoral immunodeficiencies. Among other causes, three types of diseases may induce defective antibody production: 1/B cell neoplasias (e.g. multiple myeloma, chronic lymphocytic leukemia...) 2/renal diseases (nephrotic syndrome, renal insufficiency) and 3/various infectious diseases, including AIDS. Some principles of prevention and treatment of secondary humoral immunodeficiencies are given.

Hematologic Diseases↗
PubMed1991

Humoral immunity against tick-borne encephalitis virus following manifest disease and active immunization.

Humoral immunity against tick-borne encephalitis virus (TBEV) in patients with a well-documented history of naturally acquired tick-borne encephalitis (TBE) was compared with immunity resulting from vaccination in a carefully controlled immunization programme. The vaccination study was performed with a highly purified, inactivated virus particle vaccine and the immune response was followed by tracing the course of IgG antibody formation in an enzyme-linked immunosorbent assay and a neutralization assay. It was shown that this TBE vaccine induced a strong immune response. TBE IgG antibody titres measured after three vaccinations were of the same order of magnitude as those determined in patients recovered from manifest TBE.

Adult↗
PubMed1991

Comparative immunotoxicity of 2,2'-dichlorodiethyl sulfide and cyclophosphamide: evaluation of L1210 tumor cell resistance, cell-mediated immunity, and humoral immunity.

The immunotoxicity of 2,2'-dichlorodiethyl sulfide (sulfur mustard, SM), on humoral and cell-mediated immunity was compared with that of the nitrogen mustard 2-[bis(2-chloroethyl)amino]tetrahydro-2H-1,3,2-oxazophosphorine 2-oxide (cyclophosphamide, CP). SM and CP had similar effects on thymic and splenic weights, spleen cell number, and the formation of antibody producing cells to sheep red blood cells (sRBC) when examined 5 days after exposure, but differed in their effects on body weights. Although there were no differences in the delayed hypersensitivity response to keyhole limpet hemocyanin, CP and SM had different effects in the L1210 tumor cell allograft rejection assay. CP, but not SM, decreased the 28 day survival rate of allogeneic mice exposed to a sublethal L1210 tumor challenge. The differing effects on survival to the L1210 tumor challenge could not be attributed to a direct cytotoxic effect of SM on the L1210 tumor cells as SM did not increase the survival rate or median survival time of syngeneic mice exposed to a lethal L1210 tumor cell challenge. In summary, SM and CP had immunosuppressive effects in the humoral immune assay. Although neither compound suppressed the delayed hypersensitivity response, CP was found to suppress host resistance to L1210 tumor cells.

Animals↗
PubMed1978

Renal transplantation and viral infections. IV. A survey of herpes simplex virus excretion in relation to cellular specific immunity and humoral immunity among renal transplant recipients.

Fourteen renal transplant recipients were screened systematically for HVH virus infection, cellular and humoral HVH immunity and general cellular immunity evaluated by PHA response. This study demonstrates significant correlation between humoral and cellular responses to HVH before graft and virus isolation after graft. This virus excretion occurred simultaneously with a PHA response peak. Neither significant drops in cellular general or specific HVH immune response nor correlation between acute rejection episode and any studied parameters were observed.

Adult↗
PubMed1975

[Lymphocytes. Roles in cellular immunity and humoral immunity].

The lymphocytes are now considered as ubiquitous cells which play a role in delayed hypersensitivity, the rejection of grafts and antibody synthesis. The lymphocytes are essential in the immune process, for they may both recognise the antibody and initiate the response. They act either by themselves or after differentiation into specialised cells and, usually, in coordination with other cells with phagocytic functions. After briefly recalling the morphology, localisation, circulation, sites of production and heterogeneity of the lymphocytes, the authors discuss their function, describe lymphocytic transformation, and the role of T lymphocytes in delayed hypersensitivity, in the rejection of grafts and the direct cytotoxic effect. Antibody synthesis with B lymphocytes and the intervention of mononucleated cells with phagocytic activity, the cooperation of T lymphocytes are developed. The exploration of lymphocytic functions includes the recognition of an antigen by the lymphocyte, fixation of marked antigens, rosette formation, the demonstration of delayed hypersensitivity (inhibition of macrophage migration, cytotoxicity, skin tests), the estimation of antibodies and measurement of lymphocyte transformation. Certain factors, due to antigen-host reaction, regulate the lymphocytic immune reaction. One may experimentally intervene by immunostimulation and immunosuppression.

Antibody Formation↗
PubMed1979

Augmentation of the in vitro humoral immune response by pharmacologic agents. I: An explanation for the differential enhancement of humoral immunity via agents that elevate cAMP.

Agents that elevate intracellular concentrations of cAMP in cultured spleen cells can augment the in vitro 19s humoral immune response to SRBC. DBcAMP and 8BrcAMP were more effective than MIX, CT, PGE1, or ISO in producing the enhanced PFC response, when they were present only during an early stage of immune induction. The thesis is presented that the differential ability of these agents to augment humoral immunity results from their relative ability to maintain elevated concentrations of intracellular cAMP. Studies on the cellular mechanism by which cAMP elevation produces immune enhancement reveal that DBcAMP effects are on a T-cell-deficient population of murine spleen cells (predominantly B cells and macrophages). In addition, we showed that DBcAMP cannot replace the need for helper T cells in the induction of the PFC response to SRBC. Taken collectively, these results suggest that cAMP may be an important immunoregulatory signal, and that a variety of pharmacologic agents that modulate the induction of the humoral immune response may operate via this as a final common biochemical pathway.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Lead and immunity: II. Suppression of humoral immune response to Hymenolepis nana in mice.

Serum protein changes in mice treated for varying durations with lead nitrate and subsequently infected with 1000 H. nana eggs were compared with their counterpart controls, only treated and only infected groups. Decreased values of beta and gamma globulins in all the experimental groups along with higher worm recoveries indicate suppression of humoral immune response by lead in association with higher worm recoveries indicate suppression of humoral immune response by lead in association with the cellular components since these globulins are known to contain antibodies. Lead treatment for a duration of 45 days proved to be most effective in suppressing the immune response.

Animals↗
PubMed1976

Experimental stimulation of cell-mediated immunity without concomitant stimulation of humoral immunity in graft-versus-host immunosuppressed mice.

The immunosuppressive effect of the graft-versus-host (GVH) reaction was studied in CBA X A F1 (CAF1) mice which had been rendered immunologically unresponsive by the injection of parental A strain lymphoid cells (GVH mice). Suppression of both cell-mediated and humoral immune responses was demonstrated by the prolonged survival of C57BL/6 (B6) skin allografts and by the inability of GVH mice to produce detectable antibody following stimulation with sheep erythrocytes (SRBC). Appropriate stimulation of GVH mice induced cell-mediated immune reactions to xeno- and allogeneic antigens while the humoral immune responses to the same antigens remained suppressed. Multiple challenges of the GVH mice with B6 tissue caused a rapid rejection of subsequent B6 skin grafts but failed to stimulate the production of any detectable antibodies to B6 allotransplantation antigens. Sensitization of GVH mice with SRBC in Freund's complete adjuvant stimulated a delayed hypersensitivity response to SRBC, although no humoral response to SRBC could be detected, even after three challenges with SRBC. The experimental results are discussed in terms of a proposed model for GVH-induced immunosuppression.

Animals↗
PubMed1991

Immune response gene regulation of the humoral immune response to Porphyromonas gingivalis fimbriae in mice.

Among various strains of mice immunized orally with Porphyromonas gingivalis fimbriae and adjuvant GM-53 in liposomes, BALB/c and DBA/2 mice (H-2d) were found to be high responders to the fimbriae, CBA/J and C3H mice (H-2k) were intermediate, while C57BL/6 mice were low responders in terms of serum IgG and salivary IgA responses. Furthermore, humoral immune responses were examined using congeneic mice of B10 background showing different H-2 haplotypes, and it was revealed that B10.D2 mice (H-2d), followed by B10.BR (H-2k), responded well to antigenic stimulation of the fimbriae, while C57BL/10 mice (B10, H-2b) were low responders to the fimbriae. Hybrids between BALB/c and C57BL/6 mice were found to reflect a phenotype of low responders. Thus, the humoral immune responses to P. gingivalis in mice are restricted by H-2 haplotype.

Animals↗
PubMed1991

[Experimental study of schistosome immune RNA on transfer of cellular and humoral immunity to normal mice].

The present paper reported the extraction of immune RNA (iRNA) from spleen cells of Schistosoma japonicum infected rabbits and the activity of this schistosome iRNA (SiRNA) on transfer of cellular immunity and humoral immunity using macrophage migratory inhibition test (MMIT) and Dot-ELISA. The results indicated that specific cellular immunity could be transferred to normal mice by SiRNA either via in vivo or in vitro sensitization. Intraperitoneal inoculation of SiRNA to normal mice may result in production of specific antibodies.

Animals↗
PubMed1987

Enkephalins and immunity. I: In vivo suppression and potentiation of humoral immune response.

BALB/c mice and Wistar rats immunized with sheep red blood cells and ovalbumin were treated intraperitoneally with different doses of methionine-enkephalin, leucine-enkephalin, and naloxone. Large doses of enkephalins (10-5 mg/kg b.w.) induced a significant decrease in hemolysin-forming cell response and production of hemagglutinating antibody. Immunosuppression induced by enkephalin was dose-dependent. In rats met-enkephalin was a more potent immunosuppressor than leu-enkephalin. Rats injected with 2.5 mg/kg b.w. of enkephalins into the lateral ventricle of the brain showed more pronounced immune suppression than did animals treated intraperitoneally with 5 mg/kg b.w. of enkephalins. These neuropeptides, and met-enkephalin in particular, exhibited a protective action against anaphylactic shock in rats sensitized to ovalbumin. In those animals, passive cutaneous anaphylaxis and elaboration of precipitating anti-ovalbumin antibody were considerably reduced. On the other hand, small doses of enkephalins stimulated humoral immune responses in the rat. Thus, it appears that enkephalins both suppress and potentiate immune responsiveness, depending on the dose used. As for naloxone, a large dose of this blocker of opioid receptors enhanced humoral immune reactions in the rat.

Adjuvants, Immunologic↗
PubMed1991

Humoral immune reactions in tuberculous meningitis.

Humoral immune reactions as reflected in sera and cerebrospinal fluid (CSF) of 50 patients with Tuberculous meningitis (TBM) were studied. CSFs and sera from 50 patients with nontuberculous neurological diseases were selected as controls. CSFs of patients with TBM showed high titres of circulating antimycobacterial antibodies than in nontuberculous subjects. The CSF-IgG index is significantly higher in patients with TBM. Humoral immune reaction could be applied in the laboratory diagnosis of TBM, particularly when repeated bacteriological methods are negative for M. tuberculosis in CSFs.

Antibody Formation↗
PubMed1990

Appraisal of gut lavage in the study of intestinal humoral immunity.

Direct investigation of intestinal humoral immunity requires collection of intestinal secretions or mucosal biopsy specimens, or both. A non-invasive technique of gut lavage, with a polyethyleneglycol electrolyte lavage solution as a means of collecting intestinal secretions for immunoglobulin and antibody studies, was evaluated. Fifty patients were studied--25 immunologically normal patients or volunteers, 15 patients with untreated coeliac disease, and 10 patients with active Crohn's disease. Protease inhibitors were added promptly to samples to prevent proteolysis of immunoglobulin content. Treated lavage samples were assayed by enzyme linked immunosorbent assay for immunoglobulin and antibody content. Studies of serial lavage specimens showed that early, faecally contaminated specimens contained negligible quantities of immunoglobulin, but once the specimens became clear a steady state was reached, with little variation in immunoglobulin content between serial specimens and with a uniform dilution (around 20%) of the ingested polyethyleneglycol. Gut lavage fluid IgA was predominantly secretory, comprising 92%, 81.6%, and 76.7% respectively of the total IgA gut lavage fluid content in the control, coeliac, and Crohn's groups. High values of total IgM and IgA and IgM antigliadin antibodies were detected in the coeliac group, and high values of IgG in the Crohn's disease group. This method of gut lavage is not only an effective bowel cleanser, but also a noninvasive means of obtaining intestinal secretions for the study of humoral immunity in gastrointestinal disease.

Adolescent↗
PubMed1978

The effect of ubiquinone-7 and its metabolites on the immune response. IV. Chemical structure-adjuvant activity relationship of quinonyl derivatives on humoral immune response.

The effects of the emulsion of quinonyl acids (QS-n, ES-n, KS-n) and related compounds (QSA-n) in Freund's incomplete adjuvant on the humoral immune response to bacterial alpha-amylase were assayed, and their structure-adjuvant activity relationships were discussed. All the quinonyl acids tested (500 microgram/mouse) enhanced the humoral immune response two to seven times as much as that of the control group, five weeks after immunization. 3'-Methyl and 2', 3'-double bond in the carboxy side chains of ubiquinone metabolites (Q acid-I, -II) were not essential for the adjuvant activity. The conversion of methoxyls on the quinone ring into methyls, and that of benzoquinone into phenol also did not affect the activity, but the activity seemed to depend on the carbon number of the carboxy side chain, and the prominent adjuvant activity was observed in the carboxylates having the carboxyalkyl chain of five to seven carbons. High doses (1 or 5 mg/mouse) of ubiquinone-7 and -2 enhanced the humoral immune response two to three times as much as that of the control group, and quinonyl alcohols (QSA-n) enhanced that with low dose (500 microgram/mouse).

Adjuvants, Immunologic↗
PubMed1986

Immunologic disorders: the regulation of humoral immunity.

The modulation of humoral immunity by complement and complement receptors is presented, as well as the importance of the X chromosome in immune response. Gene rearrangement and ontogeny of the immunoglobulin isotypes are discussed with regard to humoral immunodeficiency diseases.

Agammaglobulinemia↗