Modulation of Major Histocompatibility Complex (MHC) Expression by Interferons and Microbial Agents

Keller, R.; Joller, P.; Keist, Ruth; Binz, Hans; Meide, P. H. Van Der

doi:10.1111/j.1365-3083.1988.tb02422.x

Cited by 20 publications

(9 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, the use of authentic IFN-g has also produced varied results where it can restore monocyte function in patients with sepsis (6), but it increased mortality after cecal ligation and puncture (CLP) (1,7). IFN-g is an important immunomodulatory agent that activates several important macrophage functions in host defense, including tumor cell cytotoxicity, antimicrobial activity, and the induction of specific MHC antigens (8). IFN-g can directly stimulate neutrophil activation as observed by increased superoxide production and pathogen killing (9,10).…”

Section: Introductionmentioning

confidence: 99%

INTERFERON-γ INHIBITION ATTENUATES LETHALITY AFTER CECAL LIGATION AND PUNCTURE IN RATS: IMPLICATION OF HIGH MOBILITY GROUP BOX-1

Yin

Gribbin²,

Wang³

2005

Shock

View full text Add to dashboard Cite

Interferon (IFN)-gamma is an important immunomodulatory agent that is stimulated during infection to aid in host defense. However, increased IFN-gamma levels have been implicated as a mediator in various models of tissue injury and endotoxemia. We have previously shown that inhibition of IFN-gamma decreased bacterial load by accelerating peritoneal fibrin deposition in the cecal ligation and puncture (CLP) model of peritonitis. In addition, circulating inflammatory mediators such as interleukin (IL)-6 were reduced by IFN-gamma inhibition. In the present study, we show that administration of IFN-gamma antibody (1.2 mg/kg, i.v.) attenuated mortality after CLP. Administration of this antibody was able to reduce mortality when given immediately after CLP or 24 h after CLP surgery. Mortality in sepsis has been closely associated with increased release of high mobility group box-1 (HMGB1). Furthermore, it has been reported that IFN-gamma stimulates the release of HMGB1 from macrophages. Our studies showed that inhibition of IFN-gamma activity in vivo reduced the levels of HMGB1 in peritoneal fluid and serum of CLP rats 24 h after surgery. In addition, the decrease in HMGB1 was associated with an increase in tissue repair as evidenced by histological analyses. These results suggest that the attenuation of mortality in IFN-gamma antibody-treated rats was associated with a decrease in HMGB1 release.

show abstract

Section: Introductionmentioning

confidence: 99%

INTERFERON-γ INHIBITION ATTENUATES LETHALITY AFTER CECAL LIGATION AND PUNCTURE IN RATS: IMPLICATION OF HIGH MOBILITY GROUP BOX-1

Yin

Gribbin²,

Wang³

2005

Shock

View full text Add to dashboard Cite

show abstract

“…As a major activator of macrophages, IFN-␥ activates several important macrophage functions, including antimicrobial activity and antigen presentation to lymphocytes through the induction of major histocompatibility complex II (12,20). There is evidence implicating IFN-␥ in the lethality of acute endotoxemia, as the use of antibodies against IFN-␥ ameliorates lethality in this model (5).…”

mentioning

confidence: 99%

Inhibition of Gamma Interferon Decreases Bacterial Load in Peritonitis by Accelerating Peritoneal Fibrin Deposition and Tissue Repair

et al. 2003

View full text Add to dashboard Cite

Bowel perforation can lead to significant bacterial spillage, which may then cause septic peritonitis, characterized by a systemic inflammatory response and organ dysfunction. There are several reports that have shown that the development of peritoneal adhesions is dependent on inflammatory cytokine levels and that these adhesions can reduce bacterial spread, possibly by sealing off the cecum in the cecal ligation and puncture (CLP) model of septic peritonitis. There have not, however, been any studies that have utilized a strategy to accelerate tissue repair in order to seal off the injured cecum and reduce bacterial spread as well as ameliorate systemic inflammation. In the present study, we demonstrate that the administration of antigamma interferon (IFN-␥) antibody (1.2 mg/kg of body weight, intravenously) accelerated tissue repair via increased fibrin deposition 12 and 24 h after CLP in rats. This increase in fibrin deposition was associated with peritoneal adhesion 24 h after CLP and a reduction in bacterial load compared to the bacterial load of rats given irrelevant antibody. Plasma fibrin levels, however, were not altered after IFN-␥ antibody administration, suggesting that the inhibition of IFN-␥ activity specifically increased fibrin deposition to the site of injury. Furthermore, plasma interleukin-6, used as a marker of systemic inflammatory response, was reduced in CLP rats given IFN-␥ antibody compared to that found in those given irrelevant antibody. These results suggest that the early inhibition of IFN-␥ activity in the CLP model is beneficial by accelerating fibrin deposition in cecal tissue to prevent bacterial spread and reduce the systemic inflammatory response. Importantly, increased fibrin deposition in the ceca was not associated with increased plasma fibrin whereas the latter may have detrimental effects associated with coagulation disorders.

show abstract

“…3), as well as for induction of tumoricidal activity in BMMQ, low concentrations of IFN-y sufficed. In contrast, CP, as potent as IFN-y in inducing tumoricidal activity, neither affected binding of IgG nor expression of MHC class I1 molecules by BMMQ [16]. IFN-y-induced enhancement of IgG binding and of expression of MHC class I1 molecules persisted for at least 96 h (Fig.…”

Section: Properties Of the Fcyr For Monomeric Rat Iggb On Rat Bmm@mentioning

confidence: 46%

“…i n BMMQ that hid been incubated for 24 h with 5 IU IFN-ylml, binding of rat incubated for afurther 60 min at 4"Cwith affinity-purified Tab,e 1. Binding of monomeric rat, PE-conjugated anti-mouse IgG F(ab')z before analysis by FCM [16].…”

Section: Expression Of Mhc Class I1 Moleculesmentioning

confidence: 99%

Binding of monomeric immunoglobulins by bone marrow‐derived mononuclear phagocytes; its modulation by interferon‐γ

Keller

Keist

Bazin³

et al. 1990

Eur J Immunol

View full text Add to dashboard Cite

The ability of resting and activated rat bone marrow-derived mononuclear phagocytes (BMM phi) to bind monomeric rat, mouse, and human IgG was determined by means of flow cytometry. Rat IgG2b bound with high affinity (Kd approximately equal to 3 x 10(-9) M); binding was optimal at 4 degrees C and was only little affected by trypsin treatment. The other IgG bound with only low affinity (rat IgG2a, mouse and human IgG) or not at all to rat BMM phi (rat IgG1, rat IgG2c). The binding of rat IgG2b was not affected by the presence of a surplus of low-affinity binding IgG, and vice versa, indicating that high- and low-affinity IgG bind to different sites. Binding of high- and low-affinity IgG as well as expression of MHC class II molecules and of tumoricidal activity by BMM phi was markedly enhanced by rat interferon-gamma in low concentration (0.1 to 1.0 IU IFN-gamma/ml). On the other hand, heat-killed Corynebacterium parvum organisms, that were equally potent in triggering tumoricidal activity, neither enhanced the binding of IgG nor the expression of MHC class II molecules by BMM phi, suggesting that these abilities are not necessarily closely related phenomena.

show abstract

Modulation of Major Histocompatibility Complex (MHC) Expression by Interferons and Microbial Agents

Cited by 20 publications

References 31 publications

INTERFERON-γ INHIBITION ATTENUATES LETHALITY AFTER CECAL LIGATION AND PUNCTURE IN RATS: IMPLICATION OF HIGH MOBILITY GROUP BOX-1

INTERFERON-γ INHIBITION ATTENUATES LETHALITY AFTER CECAL LIGATION AND PUNCTURE IN RATS: IMPLICATION OF HIGH MOBILITY GROUP BOX-1

Inhibition of Gamma Interferon Decreases Bacterial Load in Peritonitis by Accelerating Peritoneal Fibrin Deposition and Tissue Repair

Binding of monomeric immunoglobulins by bone marrow‐derived mononuclear phagocytes; its modulation by interferon‐γ

Contact Info

Product

Resources

About