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Results for “Lymphocyte Cooperation”

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At least 19 recordsLinked to original sources
PubMed1980

Effect of Vibrio cholerae neuraminidase on the mitogen response of T lymphocytes. I. Enhancement of macrophage T-lymphocyte cooperation in concanavalin-A-induced lymphocyte activation.

Vibrio cholerae neuraminidase (VCN) enhances the immune response of lymphocytes in various systems, such as antigen- and mitogen-induced blastogenesis, mixed lymphocyte culture (MLC) and tumor-cell response. We used macrophage-depleted and reconstituted murine lymph-node T-cells to investigate the effect of VCN on macrophage-T-lymphocyte co-operation in Con-A-induced lymphocyte activation. In unfractionated lymph-node cells VCN enhanced the Con-A-induced lymphocyte activation as measured by 3H-thymidine (3H-dThd) incorporation. Removing macrophages from the cells resulted in a significantly diminished response. In addition the enhancing effect of VCN was greatly reduced. Reconstitution of the lymphocyte cultures with macrophages in increasing numbers and from various sources rstored the lymphocyte response and the enhancing effect of VCN. VCN proved to be most efficient in cultures reconstituted with normal peritoneal macrophages. Some effect was also observed using bone-marrow-derived (BM) macrophages. However, higher numbers of normal PE macrophages in the presence of VCN inhibited lymphocyte activation, and inhibition by thioglycollate-broth-induced macrophages was considerably increased by VCN. These results suggest that VCN acts by increasing the efficiency of macrophage-T lymphocyte interaction.

Animals↗
PubMed1980

Lymphocyte cooperation is required for amplification of macrophage procoagulant activity.

Murine splenic lymphoid cells have been shown to possess basal procoagulant activity. This activity was localized to most macrophages by assay of cell populations, as well as by a direct plaque assay that permitted identification of expressed procoagulant activity of individual viable cells as well as content. Both content and viable expression of procoagulant activity was markedly increased by exposure to bacterial lipopolysaccharide, reaching a maximum after 6 h. The quantitative increase in procoagulant activity content and viable expression was limited to the macrophage population. Separated populations of lymphocytes or macrophages could not be stimulated by lipopolysaccharide to increase procoagulant activity, whereas the addition of lymphocytes to macrophages at a 3-4:1 ratio maximally reconstituted the amplification of procoagulant activity. Further evidence of cellular collaboration followed from observation that only lymphocytes that had been exposed to lipopolysaccharide were capable of triggering the increase in macrophage procoagulant activity. This appears to represent a new form of lymphocyte-macrophage cooperation in an effector pathway that may participate in some forms of immunologic responses and contribute to the phenotypic features of certain immunologic tissue lesions.

Animals↗
PubMed1988

[Evaluation of lymphocyte cooperative interaction with neutrophils by the stimulation of lymphokine production in erysipelatous inflammation].

In erysipelatous inflammation lymphocytes were found to secrete lymphokine, both spontaneously and in response to in vitro stimulation with streptococcal allergen. The secreted lymphokine enhanced the oxygen-dependent metabolism of neutrophils. The lymphokine formation observed in this study depended on the clinical form of the disease. The character of the effect produced by lymphokine was determined by the initial state of target cells (macrophages).

Adolescent↗
PubMed1979

Subsets of T lymphocytes and lymphocyte cooperation. Modulation of the immunocellular response.

Recent advances in the characterization of T cell subsets suggests that the various subsets of T cells described in mice also occur in man. These various subsets of T cells can be detected by the use of appropriated antisera, co-cultivation of purified lymphoid cell preparations and differential sensitivity to radiation. Clinical applications from these new observations are now underway and it is hopeful that they should help to achieve a better understanding of the mechanisms responsible for autoimmunity, neoplasias and the various primary and secondary immunologic deficiencies.

Animals↗
PubMedDate not supplied

[Adherent cell and T lymphocyte cooperation for the "in vitro" production of Brucella-induced interferon by murine spleen cells (author's transl)].

Although Brucella is a good in vivo inducer of interferon, in vitro infection of murine spleen cells by Brucella suis has not, to the present time, led to in vitro synthesis. In the present work we show that normal spleen cells can however synthetize interferon in vitro when cultured together with adherent cells obtained from the spleens of syngeneic mice 45 min after in vivo inoculation. Induction and synthesis are thus shown to be distinct phenomena. Moreover soluble factors are shown to be involved in the induction phenomenon and T cells to be essential for synthesis. This in vitro brucella-induced interferon differs from in vivo brucella-induced interferon: its acid lability and its antigenic properties are characteristic of type II "immune" interferon.

Animals↗
PubMed1976

[Relationship between T- and B-lymphocyte cooperation and their syngeneity].

Cooperation efficiency of (CBA x C57BL/6) F1 thymocytes and CBA bone marrow cells in immune response to SRBC was compared with the syngenic combination of the same cells. Selectivity of interaction of the T- and B-lymphocytes of different origin was studied in incomplete cyclophosphamines (CBA x C57BL/6) leads to CBA chimerae, where donors were primed with SRBC and the recipients were either intact or tolerant to the given antigen. F1 T-cells proved to interact with the CAB-B-cells 10-15 times less effectively than with the syngenic B-cells. It is suggested that similarity between the antigenic structure of the cell membrane of the T- and B-lymphocytes, aiding their physical contact, increased the action efficiency of the T-mediator on the B-cell.

Animals↗
PubMed2005

CD8+ and CD20+ lymphocytes cooperate to control acute simian immunodeficiency virus/human immunodeficiency virus chimeric virus infections in rhesus monkeys: modulation by major histocompatibility complex genotype.

We have previously described two isogenic molecularly cloned simian immunodeficiency virus/human immunodeficiency virus chimeric viruses (SHIVs) that differ from one another by 9 amino acids and direct distinct clinical outcomes in inoculated rhesus monkeys. SHIV(DH12R-Clone 7), like other highly pathogenic CXCR4-tropic SHIVs, induces rapid and complete depletions of CD4+ T lymphocytes and immunodeficiency in infected animals. In contrast, macaques inoculated with SHIV(DH12R-Clone 8) experience only partial and transient losses of CD4+ T cells, show prompt control of their viremia, and remain healthy for periods of time extending for up to 4 years. The contributions of CD8+ and CD20+ lymphocytes in suppressing the replication of the attenuated SHIV(DH12R-Clone 8) and maintaining a prolonged asymptomatic clinical course was assessed by treating animals with monoclonal antibodies that deplete each lymphocyte subset at the time of virus inoculation. The absence of either CD8+ or CD20+ cells during the SHIV(DH12R-Clone 8) acute infection resulted in the rapid, complete, and irreversible loss of CD4+ T cells; sustained high levels of postpeak plasma viremia; and symptomatic disease in Mamu-A*01-negative Indian rhesus monkeys. In Mamu-A*01-positive animals, however, the aggressive, highly pathogenic phenotype was observed only in macaques depleted of CD8+ cells; SHIV(DH12R-Clone 8) was effectively controlled in Mamu-A*01-positive monkeys in the absence of B lymphocytes. Taken together, these results indicate that both CD8+ and CD20+ B cells contribute to the control of primate lentiviral infection in Mamu-A*01-negative macaques. Furthermore, the major histocompatibility complex genotype of an infected animal, as exemplified by the Mamu-A*01 allele in this study, has the additional capacity to shift the balance of the composite immune response.

Animals↗
PubMed1979

Cellular cooperation in lymphocyte activation. II. Cooperative response of human peripheral T and B lymphocytes to rabbit anti-human beta 2-microglobulin.

In the present study we attempted to clarify the effects of anti-beta 2-microglobulin (a-beta 2m) on lymphocyte activation. Neither a-beta 2m IgG fraction nor F(ab')2 had a mitogenic effect on either highly purified T or B lymphocytes alone, while their mitogenic effect was observed when T and B lymphocytes were appropriately reconstituted. When T lymphocytes were reconstituted with mitomycin C (MMC) treated B lymphocytes, a negligible decrease in the response to a-beta 2m was observed compared to the response of an untreated mixture to a-beta 2m. On the other hand, when B lymphocytes were reconstituted with MMC-treated T lymphocytes, the response was markedly diminished. It was found, moreover, that the response of T lymphocytes separated by a semipermeable membrane from MMC-treated B lymphocytes was not enhanced, while a mixture of T and MMC-treated B lymphocytes in the same chamber showed a marked response. These results lead to the conclusion that the cells responding to a-beta 2m are mainly T lymphocytes whose response is strongly enhanced by B lymphocytes, and that for the mitogenic effect of a-beta 2m direct cell-to-cell interaction between T and B lymphocytes is necessary.

Animals↗
PubMed1974

Cell interactions between histoincompatible T and B lymphocytes. VI. Cooperative responses between lymphocytes derived from mouse donor strains differing at genes in the S and D regions of the H-2 complex.

In our initial studies on the question of histocompatibility requirements in T-B-cell interactions, we found that no cooperation occurred with mixtures of T and B cells from BALB/c (H-2(d)) and A/J (H-2(a)) donors, respectively (1). These particular strains are identical for genes in the S and D regions of the H-2 complex but possess major differences at the K-end. Many differences are known to exist in the I region as well. Thus, these early data indicated that gene identities only at the D-end are insufficient to permit optimal cooperative interactions to occur under these conditions.

Animals↗
PubMed1975

Cell interactions between histoincompatible T and B lymphocytes. VII. Cooperative responses between lymphocytes are controlled by genes in the I region of the H-2 complex.

The results of this study provide compelling evidence for the existence of the gene or genes controlling optimal T-B-cell cooperative interactions in the designated I region of the H-2 gene complex. Previously, we have speculated that the relevant gene(s) involved may well be located in this region based on several observations from our earlier work in this area (3, 5, 6). Thus, in the preceding paper, we showed that T and B cells from B10.BR and A strain mice developed effective cooperative interactions in vitro to DNP-KLH in a system identical to the one reported herein. Since these mice differ for genes in the S and D regions of H-2 but are identical for K and I region genes, we were able to localize the critical genes to the K-end of H-2.

Animals↗
PubMed1981

Enumeration of alloreactive helper T lymphocytes which cooperate with cytolytic T lymphocytes.

The number of alloreactive helper T lymphocytes (HTL) which cooperate with cytolytic T lymphocytes have been quantified in a sensitive limit dilution system. Approximately 1 in 330 splenic T lymphocytes developed helper activity in response to alloantigen of a single haplotype. Most HTL appeared to cooperate nonspecifically with the cytolytic cells. A significant number of alloreactive HTL precursors recognized H-2 K or D alloantigen, but roughly 6-fold more HTL precursors responded to H-2 I, and roughly 20-fold more responded to non-H-2, presumably Mls, alloantigen. These results support the hypothesis that alloantigen encoded by the H-2 I and non-H-2 Mls regions preferentially stimulate helper T lymphocytes, while alloantigens encoded by the H-2 K and D regions preferentially stimulate cytolytic T lymphocytes.

Animals↗