Long-term follow-up of a patient with cutaneous vasculitis secondary to mixed cryoglobulinaemia and Hepatitis C virus

Kapur, N.; Tympanidis, P.; Colville, C.; Yu, Ren

doi:10.1046/j.0307-6938.2001.00942.x

Cited by 8 publications

(13 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our patient is similar to that described by Kapur et al 1 . Their patient had vasculitis with various cutaneous manifestations treated with immunosuppressants over two decades.…”

supporting

confidence: 88%

See 1 more Smart Citation

Hepatitis C virus-related cutaneous vasculitis in the absence of specific antibodies

Parodi¹,

Cozzani²,

Sorbara³

et al. 2005

Clin Exp Dermatol

View full text Add to dashboard Cite

“…Our patient is similar to that described by Kapur et al 1 . Their patient had vasculitis with various cutaneous manifestations treated with immunosuppressants over two decades.…”

supporting

confidence: 88%

“…We read with interest the intriguing case reported by Kapur et al 1 . of cutaneous vasculitis secondary to mixed cryoglobulinemia and hepatitis C virus (HCV) infection occurring in the absence of specific antibodies.…”

mentioning

confidence: 96%

Hepatitis C virus-related cutaneous vasculitis in the absence of specific antibodies

Parodi¹,

Cozzani²,

Sorbara³

et al. 2005

Clin Exp Dermatol

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

“…Here, our results suggest that B cells expressing autoAbs with higher affinity can also be activated. In clinical situations, this may lead to complications (leukocytoclastic vasculitis for example), that are known to occur during certain infectious diseases such as hepatitis C or endocarditis [34,35].A second point is that during Bb infection, some self-reactive B cells acquire a GC phenotype; and are able to upregulate Aicda gene expression and to accumulate mutations located into the recognition site of HEL 2X protein. GC reaction requires T-cell help [36,37].…”

mentioning

confidence: 99%

Chronic bacterial infection activates autoreactive B cells and induces isotype switching and autoantigen‐driven mutations

et al. 2015

View full text Add to dashboard Cite

The links between infections and the development of B-cell-mediated autoimmune diseases are still unclear. In particular, it has been suggested that infection-induced stimulation of innate immune sensors can engage low affinity autoreactive B lymphocytes to mature and produce mutated IgG pathogenic autoantibodies. To test this hypothesis, we established a new knock-in mouse model in which autoreactive B cells could be committed to an affinity maturation process. We show that a chronic bacterial infection allows the activation of such B cells and the production of nonmutated IgM autoantibodies. Moreover, in the constitutive presence of their soluble antigen, some autoreactive clones are able to acquire a germinal center phenotype, to induce Aicda gene expression and to introduce somatic mutations in the IgG heavy chain variable region on amino acids forming direct contacts with the autoantigen. Paradoxically, only lower affinity variants are detected, which strongly suggests that higher affinity autoantibodies secreting B cells are counterselected. For the first time, we demonstrate in vivo that a noncross-reactive infectious agent can activate and induce autoreactive B cells to isotype switching and autoantigen-driven mutations, but on a nonautoimmune background, tolerance mechanisms prevent the formation of consequently dangerous autoimmunity.Keywords: Affinity maturation r Autoreactive B cell r B-cell tolerance r Germinal center r Infection Additional supporting information may be found in the online version of this article at the publisher's web-site 132Sophie Jung et al. Eur. J. Immunol. 2016. 46: 131-146 Introduction B-cell receptors (BCRs) are assembled in developing B-lymphocyte precursors via a stochastic process of joining immunoglobulin (Ig) genes. These random rearrangements inevitably result in the genesis of multiple receptors that recognize self-antigens (Ags) [1]. Despite the fact that known mechanisms of central tolerance take place in the bone marrow, many self-reactive B cells escape toward the periphery [2][3][4][5]. Most of them are the so-called natural autoimmune B cells with a mature naïve phenotype, which produce-in normal individuals-small amounts of polyreactive low affinity IgM autoantibodies (Abs) devoid of somatic mutations. A recent study performed in mice also suggests that quiescent autoreactive B cells persist in the adult repertoire and could serve as a source of pathogenic autoAbs under circumstances that still have to be defined [6]. Both genetic background and environmental factors could influence B-cell maturation in a way that favors the appearance of high affinity IgG switched autoAbs. Among known environmental factors, epidemiological studies have clearly linked infections with the occurrence of autoimmune diseases in humans and in animal models [7]. In some organ-specific autoimmune diseases, this link is attributed to molecular mimicry between pathogens and self-Ags [8][9][10][11]. The role of such mechanism in the breakdown of B-cell tolerance during systemic auto...

show abstract

“…Mixed cryoglobulinemia (types II and II) is associated with connective tissue diseases, lymphoproliferative disorders (although these are more frequently seen in association with type I), and infectious diseases (Cohen et al, 1991). Mixed cryoglobulinemia is frequently a manifestation of hepatitis C infection, although these patients less frequently present with vasculitis (Kapur et al, 2002). The clinical triad of CV (mixed cryoglobulinemia with vasculitis) includes purpura induced by exposure to cold or prolonged standing, arthralgia, and weakness (Chen & Carlson, 2008).…”

Section: Cryoglobulinemic Vasculitismentioning

confidence: 99%

Pathology of the Cutaneous Vasculitides: A Comprehensive Review

Jordan¹,

Mercer²,

Phelps³

2011

Advances in the Etiology, Pathogenesis and Pathology of Vasculitis

View full text Add to dashboard Cite

Long-term follow-up of a patient with cutaneous vasculitis secondary to mixed cryoglobulinaemia and Hepatitis C virus

Cited by 8 publications

References 8 publications

Hepatitis C virus-related cutaneous vasculitis in the absence of specific antibodies

Hepatitis C virus-related cutaneous vasculitis in the absence of specific antibodies

Chronic bacterial infection activates autoreactive B cells and induces isotype switching and autoantigen‐driven mutations

Pathology of the Cutaneous Vasculitides: A Comprehensive Review

Contact Info

Product

Resources

About