Class I and class II major histocompatibility molecules play a role in bone marrow–derived macrophage development

Armstrong, Jason W.; Simske, Steven J.; Beharka, A.A.; Balch, Signe; Luttges, Marvin W.; Chapes, Stephen K.

doi:10.1002/jlb.55.5.658

Cited by 6 publications

(7 citation statements)

References 20 publications

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“…Transgenic mice, negative for MHC class II (C2D, H-2b mice) were bred in the rodent facility of the Division of Biology at Kansas State University. We confirmed the absence of MHC II molecules as described (8). Age-matched C57BL/6 (B6, H-2b) mice, also bred in the rodent facility, served as syngeneic MHC II-positive controls.…”

Section: Methodsmentioning

confidence: 76%

Staphylococcal enterotoxins bind H-2Db molecules on macrophages.

Beharka

Iandolo²,

Chapes³

1995

Proc. Natl. Acad. Sci. U.S.A.

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We screened a panel of monoclonal antibodies against selected macrophage cell surface molecules for their ability to inhibit enterotoxin binding to major histocompatibility complex class II-negative C2D (H-2b) macrophages. Two monoclonal antibodies, HB36 and TIB126, that are specific for the a2 domain of major histocompatibility complex class I, blocked staphylococcal enterotoxins A and B (SEA and SEB, respectively) binding to C2D macrophages in a specific and concentration-dependent manner. Inhibitory activities were haplotype-specific in that SEA and SEB binding to H-2k or H-2d macrophages was not inhibited by either monoclonal antibody. HB36, but not TIB126, inhibited enterotoxin-induced secretion of cytokines by H-2b macrophages. Lastly, passive protection of D-galactosamine-sensitized C2D mice by injection with HB36 antibody prevented SEB-induced death. Therefore, SEA and SEB binding to the a2 domain of the H-2Db molecule induces biological activity and has physiological consequences.

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Section: Methodsmentioning

confidence: 76%

Staphylococcal enterotoxins bind H-2Db molecules on macrophages.

Beharka

Iandolo²,

Chapes³

1995

Proc. Natl. Acad. Sci. U.S.A.

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“…Cells were evaluated for the expression of Mac-l, Mac-2, Thy 1, MHC I, and MHCII antigens using flow cytometry as described previously (2,3). Single cell suspensions of C2D, C2Dt, or B6MP102 ceils were incubated with primary antibody [Y-3, anti-K b (a generous gift from Dr. David Lee, University of Missouri, Columbia) or hybridoma HB-183 (ATCC) derived anti I-A and fluoreseeinated secondary antibody [F(ab')2; Cappel, Durham, NC] for 30 min, washed three times, and analyzed on a FACScan flow cytometer (BectonDickinson, Sunnyvale, CA).…”

Section: Methodsmentioning

confidence: 99%

“…The immature phenotype that these cell lines possess may be due to the impaired ability of macrophages to develop normally in vivo (3,36,37) or may be due to the chance isolation and transformation of "immature" macrophages. Tbe data do not allow us to make that distinction.…”

Section: -mentioning

confidence: 99%

“…opment and activation (18) as well as macrophage development (3). Interestingly, the absence or modification of MHCII appears to affect the development of macrophages (3,36,37); that is, C2D bone marrow macrophage colony formation in response to CSF-1 is significantly lower than that of wild-type bone marrow maerophages, suggesting that macrophage development may be impaired in MHCII -/-mice. Because MHCII appears to play a role in macrophage development, we questioned whether macrophage cell lines could be developed from bone mmxow ceils from MHCII -/ mice.…”

Section: Introductionmentioning

confidence: 96%

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Macrophage cell lines derived from major histocompatibility complex II-negative mice

Beharka

Armstrong

Chapes

1998

In Vitro Cell.Dev.Biol.-Animal

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Two bone-marrow-derived macrophage cell lines, C2D and C2Dt, were isolated from major histocompatibility class II negative knock-out mice. The C2D cell line was stabilized by continuous culture in colony-stimulating factor-1 and the C2Dt cell line was transformed with SV40 virus large T antigen. These cells exhibited phenotypic properties of macrophages including morphology and expression of Mac 1 and Mac 2 cell surface molecules. These cells also had comparable growth to the bone-marrow-derived macrophage cell line B6MP102. These new cell lines were not spontaneously cytotoxic and were only capable of modest killing of F5b tumor cells when stimulated with LPS and interferon-gamma, but not when stimulated with LPS alone or with staphylococcal exotoxin. C2D and C2Dt cells phagocytosed labeled Staphylococcus aureus similarly to B6MP102 cells but less well than C2D peritoneal macrophages. These cell lines secreted interleukin-6, but not tumor necrosis factor or nitric oxide in response to LPS or staphlococcal enterotoxins A or B C2D(t) cells were tumorigenic in C2D and C57BL/6J mice but C2D cells were not. These data suggest that macrophage cell lines can be established from bone marrow cells of major histocompatibility complex II-negative mice.

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“…These staphylococcal exotoxins are potent T-cell stimulants and have been called superantigens (44). Enterotoxins, exfoliative toxins, and toxic shock syndrome toxin 1 activate human, rat, and mouse macrophages to secrete tumor necrosis factor (TNF), NO-, interleukin 1 (IL-1), and IL-6 (2, 13-15, 28, 35, 36). Furthermore, macrophages become cytolytic in the presence of these exotoxins and gamma interferon (13,15).…”

mentioning

confidence: 99%

Binding and activation of major histocompatibility complex class II-deficient macrophages by staphylococcal exotoxins

et al. 1994

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Macrophages from C2D transgenic mice deficient in the expression of major histocompatibility complex (MHC) class II proteins were used to identify binding sites for superantigens distinct from the MHC class II molecule. Iodinated staphylococcal enterotoxins A and B,(SEA and SEB) and exfoliative toxins A and B (ETA and ETB) bound to C2D macrophages in a concentration-dependent and competitive manner. All four toxins increased F-actin concentration within 30 s of their addition to C2D macrophages, indicating that signal transduction occurred in response to toxin in the absence of class II MHC. Furthermore, ETA, ETB, SEA, and, to a lesser extent, SEB induced C2D macrophages to produce interleukin 6. Several molecular species on C2D macrophages with molecular masses of 140, 97, 61, 52, 43, and 37 kDa bound SEA in immunoprecipitation experiments. These data indicate the presence of novel, functionally active toxin binding sites on murine macrophages distinct from MHC class II molecules.

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Class I and class II major histocompatibility molecules play a role in bone marrow–derived macrophage development

Cited by 6 publications

References 20 publications

Staphylococcal enterotoxins bind H-2Db molecules on macrophages.

Staphylococcal enterotoxins bind H-2Db molecules on macrophages.

Macrophage cell lines derived from major histocompatibility complex II-negative mice

Binding and activation of major histocompatibility complex class II-deficient macrophages by staphylococcal exotoxins

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