IgG4 related sclerosing mastitis: expanding the morphological spectrum of IgG4 related diseases

Chougule, Abhijit; Bal, Amanjit; Das, Ashim; Singh, Gurpreet

doi:10.1097/pat.0000000000000187

Cited by 40 publications

(21 citation statements)

References 19 publications

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“…Finally, life-threatening presentations such as rupture of inflammatory aneurysms, coronary syndromes, pachymeningitis and acute neurological events have also been described occasionally [30,[40][41][42]. A comprehensive review of the organs involved by IgG4-RD, common clinical presentation and differential diagnoses is detailed in Table 1 [43][44][45][46][47][48][49][50].…”

Section: Overview Of Clinical Manifestationsmentioning

confidence: 99%

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Immunology of IgG4-related disease

Della‐Torre

Lanzillotta

Doglioni

2015

Clinical and Experimental Immunology

188

215

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SummaryImmunoglobulin G4-related disease (IgG4-RD) is a fibroinflammatory condition that derives its name from the characteristic finding of abundant IgG4 1 plasma cells in affected tissues, as well as the presence of elevated serum IgG4 concentrations in many patients. In contrast to fibrotic disorders, such as systemic sclerosis or idiopathic pulmonary fibrosis in which the tissues fibrosis has remained largely intractable to treatment, many IgG4-RD patients appear to have a condition in which the collagen deposition is reversible. The mechanisms underlying this peculiar feature remain unknown, but the remarkable efficacy of B cell depletion in these patients supports an important pathogenic role of B cell/T cell collaboration. In particular, aberrant T helper type 2 (Th2)/ regulatory T cells sustained by putative autoreactive B cells have been proposed to drive collagen deposition through the production of profibrotic cytokines, but definitive demonstrations of this hypothesis are lacking. Indeed, a number of unsolved questions need to be addressed in order to fully understand the pathogenesis of IgG4-RD. These include the identification of an antigenic trigger(s), the implications (if any) of IgG4 antibodies for pathophysiology and the precise immunological mechanisms leading to fibrosis. Recent investigations have also raised the possibility that innate immunity might precede adaptive immunity, thus further complicating the pathological scenario. Here, we aim to review the most recent insights on the immunology of IgG4-RD, focusing on the relative contribution of innate and adaptive immune responses to the full pathological phenotype of this fibrotic condition. Clinical, histological and therapeutic features are also addressed.

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Section: Overview Of Clinical Manifestationsmentioning

confidence: 99%

“…Mediastinal mass, compression of mediastinal structures, dyspnoea, chest pain Breast [50] IgG4-related mastitis Painless breast mass Abdomen and pelvis Retroperitoneum [27][28][29][30] IgG4-related retroperitoneal fibrosis (Ormond's disease)…”

Section: Pathologymentioning

confidence: 99%

Immunology of IgG4-related disease

Della‐Torre

Lanzillotta

Doglioni

2015

Clinical and Experimental Immunology

188

215

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“…IgG4‐RD and granulomatous mastitis are characterized by dense lymphoplasmacytic infiltration, similar to RDD. However, in IgG4‐RD, the number of IgG4 positive plasma cells is typically greater (IgG4/IgG ratio is >40%) and there is elevated serum IgG4 . Ganulomatous mastitis lacks emperipolesis and S100‐positive histiocytes …”

Section: Discussionmentioning

confidence: 99%

Rosai–Dorfman disease of the breast: A potential marker of systemic disease

et al. 2019

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“…The efficacy of immune suppression by steroids and methotrexate, its clinical course with periods of exacerbation and resolutions, clinical presentation with other associated immunologic findings such as erythema nodosum and bilateral ankle arthritis [9] and its self-limiting nature make autoimmunity likely to be the pivotal factor in explaining the etiology and mechanism of the disease. Moreover, a recent study showed that some forms of inflammatory mastitis are associated with immunoglobulin G4 [10]. These findings altogether point a probable immunologic mechanism underlying idiopathic GM.…”

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confidence: 95%