Reactivity of Anti-Asialo GM1 Serum With Tumoricidal and Non-Tumoricidal Mouse Macrophages

Wiltrout, Robert H.; Santoni, Angela; Peterson, EJ; Knott, D C; Overton, W. Roy; Herberman, Ronald B.; Holden, Howard T.

doi:10.1002/jlb.37.5.597

Cited by 72 publications

(43 citation statements)

References 40 publications

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“…1, 2). However, it was of concern that ASGM1 may be expressed not only in NK cells but also in some subsets of T cells and macrophages when activated (34). Therefore, we also administered anti-NK1.…”

Section: Discussionmentioning

confidence: 99%

The Development of Colitogenic CD4+ T Cells Is Regulated by IL-7 in Collaboration with NK Cell Function in a Murine Model of Colitis

Yamaji

Nagaishi

Totsuka

et al. 2012

The Journal of Immunology

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We previously reported that IL-7−/−RAG−/− mice receiving naive T cells failed to induce colitis. Such abrogation of colitis may be associated with not only incomplete T cell maintenance due to the lack of IL-7, but also with the induction of colitogenic CD4+ T cell apoptosis at an early stage of colitis development. Moreover, NK cells may be associated with the suppression of pathogenic T cells in vivo, and they may induce apoptosis of CD4+ T cells. To further investigate these roles of NK cells, RAG−/− and IL-7−/−RAG−/− mice that had received naive T cells were depleted of NK cells using anti-asialo GM1 and anti-NK1.1 Abs. NK cell depletion at an early stage, but not at a later stage during colitogenic effector memory T cell (TEM) development, resulted in exacerbated colitis in recipient mice even in the absence of IL-7. Increased CD44+CD62L− TEM and unique CD44−CD62L− T cell subsets were observed in the T cell-reconstituted RAG−/− recipients when NK cells were depleted, although Fas, DR5, and IL-7R expressions in this subset differed from those in the CD44+CD62L− TEM subset. NK cell characteristics were the same in the presence or absence of IL-7 in vitro and in vivo. These results suggest that NK cells suppress colitis severity in T cell-reconstituted RAG−/− and IL-7−/−RAG−/− recipient mice through targeting of colitogenic CD4+CD44+CD62L− TEM and, possibly, of the newly observed CD4+CD44−CD62L− subset present at the early stage of T cell development.

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Section: Discussionmentioning

confidence: 99%

The Development of Colitogenic CD4+ T Cells Is Regulated by IL-7 in Collaboration with NK Cell Function in a Murine Model of Colitis

Yamaji

Nagaishi

Totsuka

et al. 2012

The Journal of Immunology

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“…+ T, and gd T cells (9,10) and some activated form of CD4 + T cells, macrophages, and eosinophils under certain experimental conditions (11)(12)(13). Nevertheless, anti-ASGM1-mediated NK cell depletion still remains a powerful tool to analyze in vivo functions of NK cells.…”

Section: N Atural Killer Cells Provide Innate Defense Against Virusesmentioning

confidence: 99%

NK Cell-Depleting Anti-Asialo GM1 Antibody Exhibits a Lethal Off-Target Effect on Basophils In Vivo

Nishikado

Mukai

Kawano

et al. 2011

The Journal of Immunology

120

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NK cells are innate immune lymphocytes and play a key role in both innate and adaptive immunity. Their pivotal functions in vivo have been illustrated in mice by means of their ablation with NK cell-depleting Abs, particularly anti-asialo GM1 (ASGM1). In this study, we show that the whole population of basophils constitutively expresses ASGM1 as well as CD49b (DX5) as does the NK cell population and was ablated in vivo by anti-ASGM1 as efficiently as by a basophil-depleting anti-FcεRIα Ab. Anti-ASGM1–mediated basophil depletion was operative as for NK cell depletion in various mouse strains, irrespective of NK1 allotype and MHC H2 haplotype, including C57BL/6, BALB/c, C3H, and A/J mice. These results identified basophils as a previously unrecognized target of anti-ASGM1–mediated cell depletion and raised concern about possible contribution of basophils, rather than or in addition to NK cells, to some of phenotypes observed in anti-ASGM1–treated mice. Indeed, regardless of the presence or absence of NK cells in mice, anti-ASGM1 treatment abolished the development of IgE-mediated chronic cutaneous allergic inflammation as efficiently as did the treatment with basophil-depleting Ab. Given the fact that basophils have recently been shown to play crucial roles in a variety of immune responses, our finding of the off-target effect on basophils issues a grave warning about the use of anti-ASGM1 and underscores the need for careful interpretation of phenotypes observed in anti-ASGM1–treated mice.

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“…1 , such as activated macrophages 30 and a subpopulation of cytotoxic T cells, 31 and elimination of these cells might also have contributed to the loss of therapeutic efficacy seen in Figure 6.…”

Section: Requirement Of Nk Cells For Antitumor Activity In Vivomentioning

confidence: 99%

Folate receptor-targeted immunotherapy: Induction of humoral and cellular immunity against hapten-decorated cancer cells

Sega

Low

2005

Int. J. Cancer

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We previously exploited the frequent overexpression of folate receptors on cancer cells to decorate malignant cell surfaces selectively with folate-hapten conjugates. In antihapten-immunized hosts, this targeted localization of foreign haptens to tumor cells led to rapid accumulation of autologous antihapten IgG, which in turn yielded potent antitumor activity upon stimulation with cytokines (IL-2, IFN-a). In an effort to understand the effector mechanisms responsible for tumor regression, we have now investigated the involvement of both humoral and cellular immune components in the tumor destruction process. We report that the dependence of therapeutic efficacy on folate-hapten concentration is bimodal, suggesting that the conjugate must bridge between a cell surface FR and an antihapten IgG in order to mediate killing. Studies with cancer cells in vitro further demonstrate that folatefluorescein-marked tumor cells are killed primarily by antibodydependent cellular cytotoxicity and phagocytosis, with no contribution from complement-dependent mechanisms. Investigations of specific immune cell involvement also reveal that asialo-GM1 1 -natural killer cells, macrophages, CD41 T cells and CD8 1 T cells contribute significantly to recognition/removal of the cancer mass, and that elimination of these cell types markedly compromises the therapy. Because the initial antibody-dependent stage of tumor cell killing is shown to lead to a long-term antibody-independent cellular immunity that involves both CD4 1 and CD8 1 T cells, we propose that F c receptor-expressing immune cells not only initiate destruction of the IgG-marked tumor cells, but also participate in presentation of endogenous tumor antigens in a manner that leads to long-term cellular immunity. ' 2005 Wiley-Liss, Inc.

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Reactivity of Anti-Asialo GM1 Serum With Tumoricidal and Non-Tumoricidal Mouse Macrophages

Cited by 72 publications

References 40 publications

The Development of Colitogenic CD4+ T Cells Is Regulated by IL-7 in Collaboration with NK Cell Function in a Murine Model of Colitis

The Development of Colitogenic CD4+ T Cells Is Regulated by IL-7 in Collaboration with NK Cell Function in a Murine Model of Colitis

NK Cell-Depleting Anti-Asialo GM1 Antibody Exhibits a Lethal Off-Target Effect on Basophils In Vivo

Folate receptor-targeted immunotherapy: Induction of humoral and cellular immunity against hapten-decorated cancer cells

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