Rat monoclonal antibodies

Bazin, Hervé; Cormont, F.; Xhurdebise, L M

doi:10.1007/bf00481713

Cited by 8 publications

(7 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although XMG-1.2 mAb possessed more potent IFN-y-neutralizing activity both in vitro and in vivo than AN-18 mAb, it turned out to be less effective in modulating CIA. This differential effect is unlikely to be attributable to different half-lives of rat isotypes (IgG1 and IgG2a for XMG-1.2 and AN-18, respectively), since rat serum IgGl was reported to have a life span at least twofold greater than that of IgG2a [38]. It is possible that the activity of the mAb is dependent upon its affinity for its ligand.…”

Section: Discussionmentioning

confidence: 85%

Biphasic effect of interferon‐γ in murine collagen‐induced arthritis

et al. 1995

View full text Add to dashboard Cite

Interferon-gamma (IFN-gamma) exerts both enhancing and suppressing influences on collagen-induced arthritis (CIA), depending on the route and protocol of administration. To study the role of IFN-gamma on the autoimmune process of CIA, we treated DBA/1 mice with two different rat monoclonal antibodies (mAb) to murine IFN-gamma. Treatments, given twice weekly for 4 weeks, consisted of intraperitoneal injections of either mAb. In early treatments, starting from the day of immunization with type II collagen (CII), the severity of arthritis was reduced in both groups of anti-IFN-gamma-treated mice compared with control groups. Moreover, anti-CII antibody levels decreased in the sera of these mice. CIA was also down-regulated in mice treated from days 14 or 28 post immunization. In contrast, late treatments with anti-IFN-gamma mAb either induced aggravating effects, or did not affect the course of the disease. On the other hand, administration of high doses (8 x 10(4) U three times/week) of rat recombinant IFN-gamma exerted a transient increase of CIA severity. These findings suggest that IFN-gamma may play a critical role during both the induction and the course of CIA, first enhancing the immune response, and then regulating the arthritis process.

show abstract

Section: Discussionmentioning

confidence: 85%

Biphasic effect of interferon‐γ in murine collagen‐induced arthritis

et al. 1995

View full text Add to dashboard Cite

show abstract

“…IR202, [R595 and IR418 are respectively rat monoclonal Ig of the IgM-K. igGl-K and lgG2a-K isotype produced by different immunocytomas [19], These antibodies are of the IgK-la allotype; they were produced in ascitic fluid on LOU/C.IgKlb(OKA) rat (allotype IgK-lb) and immunopurified on MARK-3 (mouse MoAb against rat Ig«;Ia light chain) Sepharose [201. MARK-I is a mouse MoAb (IgGl-K) specific for rat n light chain, MARG2a-l and MARG2a-8 are mouse MoAb (IgGI-«) specific for non-overlapping epitope on rat IgG2a molecules [21]. These MoAb were all developed in our laboratory and are commercially available (Serotec, Kidlington.…”

Section: Methodsmentioning

confidence: 99%

In Vivo Study of mIgM and mIgD Cross‐Linking on Murine B Cells

Denis¹,

Macedo-Soares²,

Latinne³

et al. 1994

Scand J Immunol

Self Cite

View full text Add to dashboard Cite

In this study, we have analysed in mice the effects on the immune response of in vivo treatment with different rat monoclonal antibodies (MoAb) against IgM and IgD. Although the effects of IgD cross-linking have been studied already, no attempt has been made to characterize the effects of in vivo IgM crosslinking, probably because of the higher IgM serum levels compared to IgD. We have used a panel of nine monoclonal rat anti-mouse IgM and three anti-IgD antibodies and we have characterized their isotypes, avidities, immunoglobulin (Ig) cross-linking and internalization abilities. Our results show that injection of mice with some rat MoAb against IgM led to an important decrease of IgM serum level and internalization of membrane IgM (mIgM) on almost all B cells. Similarly, treatment with a high-avidity anti-IgD antibody induced disapperance of mIgD on B cells. Treatment with rat MoAb against IgM or IgD led to a synthesis of specific antibodies and there was a direct relationship between the Ig internalization abilities of rat MoAb and the induction of specific antibody production. Finally, treatment with a high-avidity rat MoAb against IgD induced a polyclonal IgE and IgG1 secretion. The significance of these results on mIg receptor functions is discussed.

show abstract

“…FITC anti-BrdU was purchased from BD Immunocytometry Systems (San Jose, CA). HB␦7, also known as LO-MD-7 (rat IgG2a anti-mouse IgD) (29,30), was provided by H. Bazin (Brussels, Belgium). Alkaline phosphatase conjugated to streptavidin was purchased from Jackson ImmunoResearch (West Grove, PA).…”

Section: Abs and Immunological Reagentsmentioning

confidence: 99%

IL-4 Promotes Stat6-Dependent Survival of Autoreactive B Cells In Vivo Without Inducing Autoantibody Production

Morris

Dragula

Finkelman

2002

The Journal of Immunology

View full text Add to dashboard Cite

Persistent cross-linking of hen egg lysozyme (HEL)-specific B cell membrane Ig (mIg) in double transgenic mice that express soluble HEL as a self Ag (HEL-Ig mice) decreases B cell mIgM expression, responsiveness, and life span. Because in vitro treatment with IL-4 inhibits T cell apoptosis through a Stat6-independent mechanism, increases mIg expression, and suppresses activation-induced B cell death, we studied IL-4 effects on B cell mIg expression, survival, and Ab secretion in Stat6-sufficient and deficient HEL-Ig mice. IL-4 treatment nearly normalized B cell number and greatly increased the percentage of mature B cells in HEL-Ig mice, but failed to normalize mIgM expression or spontaneous LPS-induced IgM secretion. IL-4 effects on B cell survival and maturation were CD4+ T cell independent, but Stat6 dependent, and did not involve receptor editing. IL-4 had to be present while B cells were generated to have a detectable effect on autoreactive B cell survival; however, the survival of B cells generated in the presence of IL-4 was substantially increased even after IL-4 was withdrawn. These observations suggest that: 1) activation-induced B cell death and anergy are independent processes; 2) B cells that survive to maturity develop increased resistance to Ag-induced deletion; and 3) IL-4 promotes B and T cell survival through different mechanisms.

show abstract

Rat monoclonal antibodies

Cited by 8 publications

References 6 publications

Biphasic effect of interferon‐γ in murine collagen‐induced arthritis

Biphasic effect of interferon‐γ in murine collagen‐induced arthritis

In Vivo Study of mIgM and mIgD Cross‐Linking on Murine B Cells

IL-4 Promotes Stat6-Dependent Survival of Autoreactive B Cells In Vivo Without Inducing Autoantibody Production

Contact Info

Product

Resources

About