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Biomedical subjects

M K Hoffmann

Publications and source records attributed to M K Hoffmann.

At least 91 records · Page 5Linked to original sources
PubMed1979

Macrophage factor controlling differentiation of B cells.

Peritoneal macrophages of the mouse produce, in response to cell wall components of Gram-negative bacteria (lipopolysaccharide and lipoproteins), a factor that causes antigen-stimulated B cells of differentiate into antibody-producing cells. Unlike lipopolysaccharide, this factor is not mitogenic for B cells. Production of the macrophage factor does not depend on participation of T cells or other accessory cells since it is readily produced by several cloned macrophage cell lines as well as by peritoneal macrophages of athymic nude mice. The factor is active only in conjunction with antigen. T cells, although apparently not necessary, amplify its effect. The factor induces phenotypic differentiation of B cell precursors as selectively as thymopoietin induces differentiation of prothymocytes.

Animals↗
PubMed1979

Helper T cell-replacing factors secreted by thymus-derived cells and macrophages: cellular requirements for B cell activation and synergistic properties.

The biologic activities of helper T cell-replacing factors derived from concanavalin A-stimulated murine T cells (TRF-T) and from lipopolysaccharide-activated macrophages (TFR-M) have been compared. TRF-T stimulates immune responses to heterologous erythrocyte antigens (SRBC and BRBC) in T cell-depleted spleen cultures but not in macrophage-depleted spleen cultures. TRF-M stimulates immune responses in both T cell-depleted and macrophage-depleted spleen cultures. Under conditions where LPS stimulates the release of TRF-M from cultures of activated macrophages, TRF-t has no effect on TFR-M production. Thus. TRF-T does not appear to function by stimulating the release of TRF-M from macrophages. In macrophage-depleted spleen cultures, saturating concentrations of TRF-T and TRF-M when mixed together exhibit striking synergistic effects on the induction of immune responses to erythrocyte antigens. The kinetics of the synergistic effects of TRF-M and TRF-T are consistent with an effect of TRF-M on the production of TRF-T sensitive B cells.

Animals↗
PubMed1978

Polyclonal activation of CR+ and CR- B lymphocytes: the kinetics of initiation of DNA and immunoglobulin synthesis by lipopolysaccharide.

B cells that carry the complement receptor (CR+) were separated from B cells that lack the complement receptor (CR-) by velocity sedimentation or by passage through C-coated Sephadex columns. The kinetics of responses to bacterial lipopolysaccharide (LPS) in both B cell subpopulations were determined in three assay procedures: 1) incorporation of radioactive thymidine into DNA; 2) incorporation of radioactive leucine into immunoglobulin; 3) enumeration of cells forming polyclonal antibody to the 2,4,6-trinitrophenyl hapten. Although both subpopulations of B cells responded to LPS, they differed in the time course. CR- B cells responded with a delay of approximately 24 hr as compared with the response of CR+ B cells. The implications to the ontogenetic status of CR+ and CR- B subpopulations are discussed.

Animals↗
PubMed1978

Serum from LPS nonresponder C3H/HeJ mice does not support the formation of functional EAC reagents.

Serum from C3H/HeJ mice in contrast to serum from other mouse strains does not convert EA into EAC. A factor in supportive serum permits nonsupportive C3H/HeJ serum to produce a functional EAC-rosetting reagent. This factor is heat stable. Its concentration in serum parallels the sensitivity of mice to LPS. It is absent or inoperative when sensitivity is reduced on a genetic basis and increased when sensitivity is increased by treatment with BCG.

Animals↗
PubMed1977

B-cell activation by lipopolysaccharide. Distinct pathways for induction of mitosis and antibody production.

The role played by macrophages in two effects of lipopolysaccharide (LPS) on the immune system of the mouse-substitution for helper T cells and induction of B-cell mitosis-has been investigated. C3H/HeJ mice are unresponsive and do not produce (as other strains do) antibody to 2,4,6-trinitrophenol (TNP) conjugated with autologous mouse erythrocytes (MRBC-TNP) in the presence of LPS. We found that C3H/HeJ spleen cells produce antibody to MRBC-TNP when (a) LPS and macrophages from LPS-responsive C3HeB/FeJ mice or (b) tumor necrosis serum ([TNS] induced by LPS in responsive mice) are added. The mitotic response was not restored. The findings suggest that adjuvanticity and mitogenicity represent distinct pathways of B-cell activation by LPS, subject to different regulatory mechanisms.

Adjuvants, Immunologic↗
PubMed1977

The Ly phenotype of suppressor T cells arising in mice subjected to a graft-versus-host reaction.

T cells with helper and suppressor functions arising during graft-versus-host reaction (B6 vs. BDF1) have been characterized with respect to their Ly surface antigens. Helper cells were found to express the phenotype Ly 1+2- and suppressor cells the phenotype Ly 1+2+. Ly 1-2+ T cells had no suppressive effect in this system. T cells of the host did not contribute to either activity.

Animals↗
PubMed1977

Endotoxin-induced serum factor controlling differentiation of bone-marrow-derived lymphocytes.

Serum from bacillus Calmette-Guerin-infected mice injected with endotoxin induces the appearance of surface immunoglobulin, Ia antigen, and complement receptor on the surface of precursor bone-marrow-derived (B) cells. While endotoxin itself causes phenotypic conversion of both thymus-derived (T) cells and B cells in vitro, the endotoxin-induced serum factor was found to be a selective inducer of B cell differentiation. Spleen cells rendered immunodeficient by removal of B cells bearing the complement receptor regained the capacity to cooperate with helper T cells and to produce antibody against red cell antigens in vitro upon upon addition of the serum factor to the culture medium. Thus, a factor that controls selective phenotypic and functional differentiation of B cells has been identified and can now be characterized,

Animals↗
PubMed1977

Suppressor T cells arising in mice undergoing a graft-vs-host response.

We investigated the ability of mice to generate antibody-forming cells when undergoing a graft-vs-host reaction. (C57BL/6 X DBA/2)F1 mice (BDF1) injected with C57BL/6 spleen cells generated suppressor T cells which inhibit antibody synthesis by BDF1 spleen cells in vitro. These T cells arose from the donor inoculum. They differ from helper T cells in size and they act directly on antigen reactive B cells. The suppressor T cells were specifically directed against components of the H-2 region of the reciprocal parental strain (DBA/2 = H-2d) in the hybrid F1 mouse.

Animals↗
PubMed1977

Induction of phenotypic lymphocyte differentiation in LPS unresponsive mice by an LPS-induced serum factor and by lipid A-associated protein.

Spleen cells from C3H/HeJ mice are known to be unresponsive to mitogenic stimulation by LPS. We show here that T and B cell precursors of C3H/HeJ mice are unresponsive to induction of differentiation by LPS. Phenotypic differentiation of C3H/HeJ lymphocytes can be induced with DB-cAMP, Lipid A-associated protein, and with a serum factor induced by LPS in LPS responder strains.

Animals↗
PubMed1976

Macrophage requirements of CR- and CR+ B lymphocytes for antibody production in vitro.

A Sephadex G-10 column coated with antigen-antibody complexes and complement retains complement receptor-bearing (CR+) mouse spleen cells. The effluent is rich in thymus-derived cells (T cells), and contains bone marrow-derived cells (B cells) which carry surface immunoglobulin (Ig), Ir-associated antigen (Ia), and Fc receptors, but no complement receptors (CR-). Although both unfractionated and CR- B cell populations are capable of producing antibody to red cell antigens, they differ in their requirements for the initiation of the response. Unfractionated B cells cooperate with primed as well as unprimed helper T cells; macrophages are required for this cooperation but can be replaced by 2-mercaptoethanol. CR- B cells cooperate with primed but not with unprimed T cells provided macrophages are added to cultures. After addition of culture supernatant from BCG-activated macrophages CR- B cells cooperate with both unprimed and primed T helper cells.

Animals↗
PubMed1975

Suppression and enhancement of the T cell-dependent production of antibody to SRBC in vitro by bacterial lipopolysaccharide.

LPS induced the production of antibody to sheep red blood cells (SRBC) in cultures of spleen cells from normal and T cell-depleted mice, and addition of SRBC to the cultures enchanced this T cell-independent response very little. By contrast, the T cell-dependent production of antibody to SRBC in vitro was suppressed when lipopolysaccharide (LPS) was added at the time when the spleen cells were cultured. Later addition of LPS to spleen cell cultures caused enhancement of antibody production, but only when LPS had not been added before. Addition of T cells that had been primed with SRBC in vivo did not reverse the LPS-induced suppression of antibody production. The data are interpreted to mean that either B cells are rendered incapable of receiving T cell signals in the presence of LPS or that LPS interferes with the appropriate association of cellular components which cooperate in the immune response to SRBC.

Animals↗
PubMed1975

Ly antigens: markers of T cell function on mouse spleen cells.

By the use of Ly antisera and complement it is possible to remove subpopulations of mouse T cells from spleen cell suspension. It is shown that these Ly antisera are specific for the Ly alleles carried by the cells. Helper cells from primed or unprimed mice and cells which respond to Con A express Ly-1 antigen but little or no Ly-2 antigen (Ly-1+ phenotype) whereas cells which respond to PHA express both Ly-1 and Ly-2 antigens (Ly-1+2+ phenotype).

Animals↗
PubMedDate not supplied

Mls and the helper T-cell repertoire. I. Mls as a regulator of T-helper cell activation.

We provide evidence that the Mls reaction involves a broad cross-section of the helper cell population. In addition to those cells reacting overtly to Mls stimulatory spleen cells, there is a second large population of helper cells that are affected by an Mls difference. This latent Mls effect is manifested by either synergy or antagonism in mitogen-mediated, Ia-dependent T-cell activation, depending on Mlsa or Mlsb phenotypes of stimulator cells, respectively. Our data can be explained by attributing to Mls alleles the function of differential regulation of autoreactivity of T cells. The results show that the concept of the Mls exerting a negative signal deserves serious consideration.

Animals↗