Immunologic responsiveness of the C3H/HeJ mouse: differential ability of butanol-extracted lipopolysaccharide (LPS) to evoke LPS-mediated effects.

Goodman, M G; Parks, D E; Weigle, W O

doi:10.1084/jem.147.3.800

Cited by 22 publications

(10 citation statements)

References 47 publications

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“…1 B), thus demonstrating that the C3H/HeJ spleen cells were able to manifest an adjuvant response when appropriately stimulated. Our results concerning polyclonal activation by Bu-LPS and by high concentrations of Ph-LPS were in agreement with previous findings by others (9,35).…”

Section: Resultssupporting

confidence: 94%

Cellular requirements for lipopolysaccharide adjuvanticity. A role for both T lymphocytes and macrophages for in vitro responses to particulate antigens.

McGhee

Farrar

Michalek

et al. 1979

The Journal of Experimental Medicine

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It has been known for over 30 yr that gram-negative bacteria enhance immune responses to vaccines in man (1) and that the active adjuvant component is cell wall lipopolysaecharide (LPS) 1 (2). However, the precise mechanism by which LPS mediates its adjuvant effect has not yet been resolved.Because LPS is a potent B-cell mitogen, a polyclonal B-cell activator, and acts as a T-independent antigen, several investigators have suggested that the adjuvant properties of LPS are most easily ascribed to a direct effect of LPS on the B cells (3-6). Because LPS reverses tolerance to immunity, even in the presence of T-suppressor cells, this has been taken as further proof that LPS enhances B-cell responses (5, 7). LPS can also bypass the requirement for T-helper cells by facilitating immune responses in mice given haptenated, homologous erythrocytes (8, 9). Finally, the lack of tolerance reversal to human gamma globulin by LPS in C3H/HeJ mice (whose B cells are unresponsive to LPS) has been taken as evidence that potentiation is occurring at the level of the B cell (3, 10, 11).Alternatively, a number of studies have suggested that the adjuvant properties of LPS are best explained through activation of T cells (12)(13)(14)(15)(16)(17). Allison and Davies (12), utilizing both thymectomized mice and mice treated with anti-lymphocyte serum, demonstrated that LPS adjuvanticity required normal T-cell populations. In a series of experiments, Katz and coworkers (13-15) also provided evidence for a T-cell requirement during LPS-mediated augmentation of antibody responses. In the first experiments, removal of T cells from antigen-primed spleen cells before adoptive transfer and subsequent challenge abrogated the capacity of LPS to mediate its adjuvant effect (13). Subsequent studies (14, 15) provided evidence that the adjuvant effect of LPS on hapten-specific IgM, IgG, and IgE plaque-forming cell (PFC) responses was exerted on carrier primed, T-helper cell activity. More recent evidence * On sabbatical leave from the

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Section: Resultssupporting

confidence: 94%

Cellular requirements for lipopolysaccharide adjuvanticity. A role for both T lymphocytes and macrophages for in vitro responses to particulate antigens.

McGhee

Farrar

Michalek

et al. 1979

The Journal of Experimental Medicine

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“…3). This segregation of the ability to interfere with the induction of tolerance from other mechanisms of adjuvant activity has been documented previously (71) in athymic nude mice (19,20) and in the LPS-nonresponder C3H/HeJ mouse (72), with polymerized flagellin (19), LPS (20), and lipid A-associated protein (72).…”

Section: Inability Of Col Tomentioning

confidence: 97%

Induction and mode of action of suppressor cells generated against human gamma globulin. II. Effects of colchicine.

Parks¹,

Shaller²,

Weigle³

1979

The Journal of Experimental Medicine

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The ability of colchicine (Col) to interfere with suppressor cells specific for the soluble protein antigen human gamma globulin (HGG) has been examined. This interference may be the mechanism of the adjuvanticity promoted by Col. When injected into A/J mice at the appropriate time and concentration, both Col and cyclophosphamide promoted an adjuvant increase in the plaque-forming cell response to 100 micrograms of immunogenic, aggregated HGG. Col abrogated both the induction of suppressor cells when injected with 3 h of tolerization with deaggregated (DHGG) and the expression of previously induced suppressor cells when injected with the antigenic challenge. Interference with the generation and expression of antigen-specific suppressor cells had no detectable effects on the immunologic unresponsive state to HGG. Col did not interfere with the induction of tolerance at a dose (1 mg/kg) that abolished the generation of suppressor cells. Furthermore, the absence of colchicine-sensitive-suppressor cells during the establishment of tolerance had no observable effect on the duration of unresponsivness in either helper T- or B-lymphocyte populations. Finally, Col was not able to terminate the unresponsive state established by DHGG even when responsive splenic B cells could be demonstrated in tolerant animals. These data indicate that suppressor cells are not required for the establishment and maintenance of the unresponsive state to this antigen.

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“…Sultzer (30) described a mutant C3H mouse, C3H/HeJ, which appeared to be resistant to the effects of phenol-extracted LPS. Further work with this strain has shown that it is refractory to virtually all LPS-mediated effects studied, including mitogenesis and PBA (7,10,34), although this strain can respond to the butanoland trichloroacetic acid-extracted LPS (10,19) which contains a low molecular weight protein bound tightly to the lipid A moiety of LPS (endotoxin protein or lipid A-associated protein ; LAP) (18,3]). We demonstrated that all of the active preparations of the cell walls and theirfractions have the ability to induce PBAeffects on cultured spleen cells of this LPS-nonresponder strain.…”

Section: Introductionmentioning

confidence: 99%

Polyclonal B Cell Activation by Cell Wall Preparations of Gram‐Positive Bacteria

Saito‐Taki

Tanabe

Mochizuki

et al. 1980

Microbiology and Immunology

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The effects of polyclonal B cell activation (PBA) of cell walls and their cell wall fractions obtained from several kinds of gram‐positive bacteria were studied using the anti‐sheep red blood cell (SRBC) or anti‐trinitrophenylated (TNP) SRBC plaque forming cell (PFC) responses of cultured spleen cells from Balb/c, athymic nu/nu, their littermates (nu/+), C3H/He (LPS‐responder), C3H/HeJ (LPS‐non‐responder), (CBA/N × Balb/c) F1 male with an X‐linked defect in B cell function and the F1 female mice. The cell walls of Staphylococcus epidermidis (ATCC 155), Lactobacillus plantarum (ATCC 8014), Micrococcus lysodeikticus (NCTC 2665), Mycobacterium rhodochrous (ATCC 184), Streptomyces gardneri (ATCC 23911) and Nocardia corynebacteriodes (ATCC 14898) had the ability to induce polyclonal B cell responses in the spleen cells of Balb/c, nu/nu, nu/+, C3H/He and C3H/HeJ mice. The cell wall fractions prepared by enzymatic digestion from the cell walls of S. epidermidis, S. gardneri or N. corynebacteriodes were also capable of inducing polyclonal B cell responses. The responses of spleen cells from (CBA/N × Balb/c) F1 male mice to these active preparations, except the cell walls of M. rhodochrous, were much lower than those of the F1 female mice. These findings indicate that the majority of the cell wall preparations lacks PBA ability for spleen cells with the CBA/N defect, except for the cell walls of M. rhodochrous which possess this ability. The PBA‐ability of synthetic peptidoglycan, muramyl dipeptide (N‐acetylmuramyl‐L‐alanyl‐D‐isoglutamine, MDP), was also examined, and a similar activity was observed in MDP.

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Immunologic responsiveness of the C3H/HeJ mouse: differential ability of butanol-extracted lipopolysaccharide (LPS) to evoke LPS-mediated effects.

Cited by 22 publications

References 47 publications

Cellular requirements for lipopolysaccharide adjuvanticity. A role for both T lymphocytes and macrophages for in vitro responses to particulate antigens.

Cellular requirements for lipopolysaccharide adjuvanticity. A role for both T lymphocytes and macrophages for in vitro responses to particulate antigens.

Induction and mode of action of suppressor cells generated against human gamma globulin. II. Effects of colchicine.

Polyclonal B Cell Activation by Cell Wall Preparations of Gram‐Positive Bacteria

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