Rituximab in the treatment of systemic sclerosis-associated interstitial lung disease: Comment on the article by Yoo

Daoussis, Dimitrios; Andonopoulos, Andrew P.

doi:10.1007/s00296-010-1485-3

Cited by 4 publications

(2 citation statements)

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“…Studies in experimental animals and in humans with SSc have implicated the semantic role of B cells in the pathogenesis of the disease [5,13,14]. Apart from the peripheral blood, B cell infiltrates are apparent in lung tissue from SSc patients as well [15].…”

Section: Introductionmentioning

confidence: 99%

Treating scleroderma lung disease with B cell depletion

Bounia¹,

Liossis²

2020

J Transl Sci

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Systemic sclerosis (SSc) is a rare, aggressive, systemic, autoimmune disease especially because of internal (vital) organ involvement, most commonly over the last decades of the lungs. Therefore, there is an increasing need for the rheumatologist to select an effective treatment in order to improve patients' prognosis.Recent experimental data have established a role of the B cell in pathogenesis of the disease. B cell depletion, although not usually chosen as first-line treatment, has been investigated over the past decade in controlled and uncontrolled trials with satisfactory results mainly in skin involvement, but trials of B cell depletion in improving lung function do not lag behind in effectiveness compared to respective results in the skin. This review is referring to trials that have attributed B cell depletion an optimistic view of halting progression of interstitial lung disease in scleroderma.Bounia CA (2020) Treating scleroderma lung disease with B cell depletion

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Section: Introductionmentioning

confidence: 99%

Treating scleroderma lung disease with B cell depletion

Bounia¹,

Liossis²

2020

J Transl Sci

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“…The importance of these roles is supported by the therapeutic benefit gained from depleting B cells in patients with a range of autoimmune diseases. For example, patients with diseases such rheumatoid arthritis (RA) [ 71 ], type 1 diabetes (T1D) [ 72 ], anti-neutrophil cytoplasmic antibody (ANCA) vasculitis [ 73 ], multiple sclerosis (MS) [ 74 ], systemic sclerosis (SSc) [ 75 , 76 ], primary Sjögren’s syndrome [ 77 – 80 ] and systemic lupus erythematosus (SLE) [ 81 – 83 ] benefit from therapeutic depletion of B cells. Of note in this respect is that B cell-depleting therapy has a clinical benefit without significantly affecting autoantibody levels, suggesting that, perhaps, other B cell functions, including antigen presentation and cytokine production could be critical aspects of B cell involvement in the pathogenesis of the autoimmune diseases.…”

Section: Introductionmentioning

confidence: 99%

Intracellular B Lymphocyte Signalling and the Regulation of Humoral Immunity and Autoimmunity

Taher

Byström

Ong

et al. 2017

Clinic Rev Allerg Immunol

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B lymphocytes are critical for effective immunity; they produce antibodies and cytokines, present antigens to T lymphocytes and regulate immune responses. However, because of the inherent randomness in the process of generating their vast repertoire of antigen-specific receptors, B cells can also cause diseases through recognizing and reacting to self. Therefore, B lymphocyte selection and responses require tight regulation at multiple levels and at all stages of their development and activation to avoid diseases. Indeed, newly generated B lymphocytes undergo rigorous tolerance mechanisms in the bone marrow and, subsequently, in the periphery after their migration. Furthermore, activation of mature B cells is regulated through controlled expression of co-stimulatory receptors and intracellular signalling thresholds. All these regulatory events determine whether and how B lymphocytes respond to antigens, by undergoing apoptosis or proliferation. However, defects that alter regulated co-stimulatory receptor expression or intracellular signalling thresholds can lead to diseases. For example, autoimmune diseases can result from altered regulation of B cell responses leading to the emergence of high-affinity autoreactive B cells, autoantibody production and tissue damage. The exact cause(s) of defective B cell responses in autoimmune diseases remains unknown. However, there is evidence that defects or mutations in genes that encode individual intracellular signalling proteins lead to autoimmune diseases, thus confirming that defects in intracellular pathways mediate autoimmune diseases. This review provides a synopsis of current knowledge of signalling proteins and pathways that regulate B lymphocyte responses and how defects in these could promote autoimmune diseases. Most of the evidence comes from studies of mouse models of disease and from genetically engineered mice. Some, however, also come from studying B lymphocytes from patients and from genome-wide association studies. Defining proteins and signalling pathways that underpin atypical B cell response in diseases will help in understanding disease mechanisms and provide new therapeutic avenues for precision therapy.

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