Toll‐like receptor 2 and toll‐like receptor 4 expression on CD64+ monocytes in rheumatoid arthritis: Comment on the article by Iwahashi et al

Frasnelli, Matthias; So, Alexander

doi:10.1002/art.21113

Cited by 9 publications

(7 citation statements)

References 28 publications

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“…This restricted expression profile means that CD64 is a valuable target for diseases associated with abnormally high numbers of CD64 + macrophages or their progenitors. Such diseases include many chronic inflammatory diseases like rheumatoid arthritis 4 , 30 inflammatory bowel disorders 31 , 32 , 33 and systemic lupus erythematosus 34 , 35 , 36…”

Section: Discussionmentioning

confidence: 99%

Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64⁺ M1 macrophages

et al. 2016

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Classical immunotoxins compromise a binding component (for example, a ligand, antibody or fragment thereof) and a cytotoxic component, usually derived from bacteria or plants (for example, Pseudomonas exotoxin A or ricin). Despite successful testing in vitro, the clinical development of immunotoxins has been hampered by immunogenicity and unsatisfactory safety profiles. Therefore, research has focused on fully human pro-apoptotic components suitable for the development of cytolytic fusion proteins (CFP). We recently reported that human microtubule-associated protein tau (MAP) can induce apoptosis when delivered to rapidly proliferating cancer cells. Here, we describe a new fully human CFP called H22(scFv)-MAP, which specifically targets CD64(+) cells. We show that H22(scFv)-MAP can efficiently kill proliferating HL-60 pro-monocytic cells in vitro. In addition, the human CFP specifically eliminates polarized M1 macrophages in a transgenic mouse model of cutaneous chronic inflammation. Because M1 macrophages promote the pathogenesis of many chronic inflammatory diseases, targeting this cell population with H22(scFv)-MAP could help to treat diseases such as atopic dermatitis, rheumatoid arthritis and inflammatory bowel disease.

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Section: Discussionmentioning

confidence: 99%

Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64⁺ M1 macrophages

et al. 2016

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“…Previous studies have demonstrated an increased number of TLR2+ cells in different inflammatory diseases such as tuberculoid lesions of leprosy, 10 acne vulgaris 6 and rheumatoid arthritis. 11,12 Furthermore, the activation of TLR2 on monocytes ⁄macrophages in certain autoimmune and inflammatory diseases was shown to induce the production of proinflammatory cytokines, e.g. interleukin (IL)-12 and tumour necrosis factor (TNF)-a, which in turn may promote a Th1-mediated immune response.…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 2 is highly expressed in lesions of acne inversa and colocalizes with C-type lectin receptor

et al. 2008

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“…Thus far, TLR2, TLR4, TLR3 and TLR7 have been shown to be increased [24, 25], with monocytes and tissue macrophages expressing elevated levels of TLR2 and TLR4 [26], while synovial lymphocytes have been reported to have increased expression of TLR2 but not TLR4 [27]. Dendritic cells have been shown to be involved through the production of cytokines in response to ligation of TLRs.…”

Section: How Are Rf B Cells Induced To Produce Rf?mentioning

confidence: 99%

Rheumatoid Factors: Good or Bad for You?

Nowak

Newkirk

2005

Int Arch Allergy Immunol

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Background: Rheumatoid factors (RFs) are autoantibodies associated with rheumatoid arthritis. They can be detected in normal individuals, although transiently. This dichotomy has led to questions about the origins and types of RFs. Recently it has been shown that B cells that produce RFs only do so when activated by two signals, one from engagement of the B-cell receptor and the other from recognition of a pathogen-associated molecular pattern through a Toll-like receptor (TLR). These autoantibodies thus link the innate and acquired immune responses. Objective: Through a review of the literature, an examination of the current knowledge of RF induction is presented. The focus is on a discussion of a beneficial or detrimental role for RFs in normal individuals and in those with chronic disease. Results: What makes RF ‘good’ in some cases and ‘bad’ in others may reflect the type of RF produced. Low-affinity polyreactive IgM RFs are probably beneficial as they aid in the clearance of immune complexes that are more efficiently cleared, and the RF B cell can act as an antigen-presenting cell and stimulate host defense. However, large amounts of high-affinity RFs found in patients with chronic disease may be harmful by participation in a vicious cycle of autoantibody production by stimulation of self lymphocytes, and/or deposition in blood vessels thus causing vasculitis. Conclusions: Whether RFs are beneficial or detrimental depends on the context in which they are expressed, the type and amount of RF produced, whether the response is perpetuated by TLR ligation and whether other cells are stimulated either directly or indirectly by RF-positive B cells.

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Toll‐like receptor 2 and toll‐like receptor 4 expression on CD64+ monocytes in rheumatoid arthritis: Comment on the article by Iwahashi et al

Cited by 9 publications

References 28 publications

Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64⁺ M1 macrophages

Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64⁺ M1 macrophages

Toll-like receptor 2 is highly expressed in lesions of acne inversa and colocalizes with C-type lectin receptor

Rheumatoid Factors: Good or Bad for You?

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Toll‐like receptor 2 and toll‐like receptor 4 expression on CD64+ monocytes in rheumatoid arthritis: Comment on the article by Iwahashi et al

Cited by 9 publications

References 28 publications

Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64+ M1 macrophages

Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64+ M1 macrophages

Toll-like receptor 2 is highly expressed in lesions of acne inversa and colocalizes with C-type lectin receptor

Rheumatoid Factors: Good or Bad for You?

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Product

Resources

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Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64⁺ M1 macrophages

Fully human MAP‐fusion protein selectively targets and eliminates proliferating CD64⁺ M1 macrophages