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Osteoarthritis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Marc C. Hochberg, Virginia Byers Kraus, Stefan Lohmander, Ali Guermazi, Frank W. Roemer, Ali Mobasheri
Another important contributor to the process of “low-grade” inflammation in OA is the synovium (23, 33). There is evidence of cross-talk between articular cartilage, subchondral bone, and synovium (34). No less than twelve distinct synovial cell types have been identified in OA; among these are a large proportion (13%) of immune cells, including both pro-inflammatory (cytokine producing) and immune regulatory macrophages (thioredoxin-interacting protein [TXNIP] producing, an inhibitor of NF-κB activity) (34). Mechanistic evidence comes from in vitro and animal studies, and clinical evidence from studies on patients with OA (34, 35). Synovial cells, particularly type A macrophage-like synoviocytes, are likely to be the major source of pro-inflammatory mediators within the joint (36). Moreover, there are differences in the profile of pro-inflammatory cytokine production in classically activated (M1) and alternatively activated (M2) macrophages (37, 38). Macrophage polarization is an issue that may be relevant not only to emerging targeted therapies; recent findings have also demonstrated a hitherto-underappreciated role of neutrophils in the sterile inflammatory process and progression of OA with an apparent synergistic role of neutrophil and macrophage populations in the pathogenesis and worsening of OA (39) that could potentially be utilized to identify patients who may have a greater risk of more rapid disease progression, and there are ongoing efforts aimed at discriminating the different molecular endotypes and clinical phenotypes of OA (40, 41).
Effect of the combination of Typhonium flagelliforme Lodd. (Blume) and Phyllanthus niruri Linn. on the immune system
Published in Elida Zairina, Junaidi Khotib, Chrismawan Ardianto, Syed Azhar Syed Sulaiman, Charles D. Sands, Timothy E. Welty, Unity in Diversity and the Standardisation of Clinical Pharmacy Services, 2017
S.S. Pangestika, A.P. Gani, A. Yuswanto, R. Murwanti
There are several work mechanisms of macrophages related to cytokines that requires further assessment, for instance, IL-4 and IL-13 assay to identify the mechanism of alternatively activated macrophages or IL-10 production assay to assess regulatory macrophages (Weiss & Schaible 2015).
Characteristics of biological therapy in pediatric patients with Crohn’s disease
Published in Expert Opinion on Biological Therapy, 2019
Andras Tarnok, Zoltan Kiss, Orsolya Kadenczki, Gabor Veres
IFX and ADA exert their main biological effect via binding to soluble and transmembrane forms of TNF with high affinity, and neutralizing its function. TNF is a major pro-inflammatory cytokine which activates NF-κb, MAPK, and caspase signaling pathways on various cell types. IFX and ADA bind with near equal affinity to TNF and neutralize TNF dependent downstream signaling effects, therefore the different clinical efficacy profiles of these drugs are not explained by intrinsic binding property differences [8]. Besides the disruption of downstream inflammatory signaling originating from the receptor binding of soluble TNF, both drugs are capable to elicit complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity via the functional Fc region of the antibodies which bind to the transmembrane form of TNF. One of the effects elicited in an Fc dependent manner is the induction of regulatory macrophages resembling the anti-inflammatory M2 macrophage phenotype. These macrophages can inhibit ongoing immune response and promote tissue repair and resolution of inflammation. The induction and function of these effector cells are autophagy-dependent; therefore, it requires an intact autophagy pathway, however, the presence of certain risk alleles can reduce the patient’s ability to generate these macrophages [9]. Given the complex and pleiotropic downstream effects of TNF signalization, the full extent of mechanisms culminating in the alleviation of inflammation is still a matter of active research.
Effect of Adalimumab on Peripheral Blood Mononuclear Cells in Non-Infectious Uveitis
Published in Ocular Immunology and Inflammation, 2019
Karoline Walscheid, Toni Weinhage, Dirk Foell, Carsten Heinz, Maren Kasper, Arnd Heiligenhaus
A study by Herenius et al. observed a markedly decreased joint inflammation in RA patients as early as 2 weeks after adalimumab initiation, while monocyte influx to the joints was not decreased at this time point, implicating that monocyte activity or function might be modified, though absolute numbers of monocytes remain stable. 7 Additionally, it has been shown previously that adalimumab treatment induced regulatory macrophages in vitro in an Fc-dependent manner, and that T cell proliferation in a mixed lymphocyte reaction was inhibited by macrophages after adalimumab treatment. 8 It is proposed that binding of anti TNFα-antibodies to different types of Fcγ-receptors might be an important mechanism by which the clinical effect of adalimumab and infliximab is mediated. 9,10
IL-33 delays metastatic peritoneal cancer progression inducing an allergic microenvironment
Published in OncoImmunology, 2019
Alfredo Perales-Puchalt, Nikolaos Svoronos, Daniel O. Villarreal, Urvi Zankharia, Emma Reuschel, Krzysztof Wojtak, Kyle K. Payne, Elizabeth K. Duperret, Kar Muthumani, Jose R. Conejo-Garcia, David B. Weiner
Unlike other tumor locations, the peritoneal cavity is commonly exposed to gut breaching and ascending genital microorganisms, which makes it particularly sensitive to changes in innate immunity. Therefore, the peritoneal cavity has a resident population of ontogenically differentiated resident macrophages that serve as first line of defense.22 Allergic reactions are characterized by the presence of an activated macrophages, also described as wound-healing or M2a macrophages.23-25 Accordingly, we found that peritoneal macrophages presented this allergic like activated phenotype shown by an increased production of Ym-1 and IL-13 (Figure 5a&b). These macrophages also expressed the IL-33 receptor ST2 (Figure 5c), thus allowing for their direct IL-33 stimulation. These differed from the M2c regulatory macrophages or tumor-associated macrophages by a lack of expression of the regulatory cytokine IL-10 (Figure 5d). Interestingly, this phenotype was associated with decreased expression of CD40 (Figure 5e& Suppl. Figure 1c) and CD80 (Figure 5f& Suppl. Figure 1d) but an increase in CD86 (Figure 5g) compared to PBS treated mice. The differential regulation of CD80 and CD86 has been previously reported in asthmatic patients, suggesting an important role for CD86 after allergen challenge.26