The Role of Monocytes and Macrophages in Autoimmune Diseases: A Comprehensive Review

Ma, Wentao; Gao, Fei; Gu, Ke; Chen, Dekun

doi:10.3389/fimmu.2019.01140

Cited by 254 publications

(236 citation statements)

References 364 publications

(327 reference statements)

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“…They improved the survival by treating with an anti-CD40L monoclonal antibody, suggesting the suppression of CD40 and CD40L interactions probably contribute to the amelioration of lupus-like disease. [ 32 , 33 ] Considering that the patients with rs4132601 GG genotype had a significantly higher CD40L concentration, IKZF1 might affect SLE's development by maintaining high levels of CD40L. It probably provides new targets and ideas for the treatment.…”

Section: Discussionmentioning

confidence: 99%

IKZF1 polymorphisms are associated with susceptibility, cytokine levels, and clinical features in systemic lupus erythematosus

et al. 2020

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Ikaros family zinc finger 1(IKZF1) encodes a lymphoid-restricted zinc finger transcription factor named Ikaros that regulates lymphocyte differentiation and proliferation as well as self-tolerance. Increasing evidence indicates that IKZF1 could contribute to the pathogenesis of autoimmune diseases. Recent research has provided evidence that IKZF1 might correlate with Systemic lupus erythematosus (SLE), but no clear definition has been made yet. In this study, we focus on the relationship between IKZF1 polymorphisms and SLE susceptibility, cytokine levels, and clinical characteristics in the Chinese Han population. One thousand seventy-six subjects, including 400 SLE patients and 676 healthy controls, were included in this study. Three single nucleotide polymorphisms within IKZF1 containing rs4917014, rs11980379, and rs4132601 were genotyped in all subjects by an improved multiplex ligation detection reaction technique. 143 subjects from SLE patients were randomly selected for testing the levels of serum cytokines. The clinical characteristics of SLE patients were gathered and collated from medical records. The data were analyzed mainly using SPSS20.0 (SPSS lnc., Chicago, IL). Significant relationships were observed between rs4132601 and SLE susceptibility, CD40 ligand, and malar rash ( P < .001, P = .04, and P = .01, respectively). In addition, significant relationships were observed between rs4917014 and susceptibility, granzyme B level, and hematological disorder in SLE ( P = .005, P = .03 and P = .005, respectively). The results further support that IKZF1 may have an important role in the development and pathogenesis of SLE. Allele G of rs4132601 and rs4917014 is related to a decreased risk of SLE occurrence and associated with clinical features in SLE patients, including CD40 ligand level, granzyme B level, malar rash, and hematological disorder, which play important roles in disease progression.

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Section: Discussionmentioning

confidence: 99%

IKZF1 polymorphisms are associated with susceptibility, cytokine levels, and clinical features in systemic lupus erythematosus

et al. 2020

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“…Furthermore, future studies with available immune phenotyping data can help provide insight into the mechanism for the BS-induced clinical benefits observed in our study by examining phenotypical, functional, and activating properties of immune cell populations involved in the pathogenesis of AIH. [ 22 ]…”

Section: Discussionmentioning

confidence: 99%

The impact of bariatric surgery on in-patient clinical outcomes among patients with autoimmune hepatitis

et al. 2020

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Autoimmune hepatitis (AIH) is a form of liver inflammation in which immune cells target hepatocytes, inducing chronic inflammatory states. Bariatric surgery (BS) was shown to reduce inflammation in severely obese patients. We hypothesize that obese patients with AIH and BS have lower prevalence of liver-related complications and in-patient mortality compared to those without BS. The National Inpatient Sample from 2007 to 2013 was queried for hospitalizations of adults over 18 years of age with a diagnosis of AIH. Of those, hospitalizations with BS were selected as cases and those with morbid obesity as controls. Case-control 1:2 matching was done based on sex, age, race, and comorbidities. Primary outcomes were prevalence of liver-related complications and in-patient mortality. Independent risk factors of in-patient clinical outcomes were identified using multivariate regression analysis. From 137,834 hospitalizations with a diagnosis of AIH, 688 with BS were selected as cases, and 1295 were matched as controls. The prevalence of ascites was higher in the BS group compared to the control (odds ratio 1.73, 95% confidence interval (CI) 1.27–2.36). The prevalence of cirrhosis (36.8% vs 33.2%), portal hypertension (7.4% vs 10.0%), hepatic encephalopathy (10.6% vs 8.7%), and varices and variceal bleeding (3.9% vs 5.5%) was not statistically different from case controls, ( P > .05). BS was an independent risk factor for ascites (adjusted odds ratio (aOR) 1.87; 95% CI 1.36–2.56) and hepatic encephalopathy (aOR 1.42; 95% CI 1.03–1.97) but was an independent protective factor against in-patient mortality (aOR 0.21, 95% CI 0.08–0.55) once adjusted for age, sex, race, and comorbidities.

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“…These observations point towards an adaptive process through which the threshold for activation is controlled by the local environment, which in NK cells is referred to as 'education' 14,15 . This process must be extremely robust, as autoimmunity due to direct attack by NK cells and macrophages on healthy tissues is essentially unknown 16,17 . How do these immune cells achieve self-tolerance while retaining the ability to respond to unhealthy targets?…”

Section: Introductionmentioning

confidence: 99%

A quantitative model for the regulation of innate immune activation

Qin

Mace

Barton

2020

Preprint

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The immune system employs a wide variety of strategies to protect the body from infection. Cells such as natural killer (NK) cells and macrophages can recognize and eliminate targets with aberrant surface ligand expression in a manner that is not antigen-specific. This innate mechanism of activation must be tightly regulated to prevent autoimmunity. Here we introduce a quantitative model of the regulation of nonspecific activation inspired by Bayesian inference. Our model captures known behaviors of innate immune cells, including adaptation to changing environments and the development of hyposensitivity after prolonged exposure to activating signals. Our analysis also reveals a tradeoff between precision and adaptation. Maintaining the ability to adapt to different environments leads to heterogeneous responses, even for hypothetical populations of immune cells and targets that have identical surface receptor and ligand expression. Collectively, our results describe an adaptive algorithm for self/nonself discrimination that functions even in the absence of antigen restriction. The same model could also apply more broadly to the adaptive regulation of activation for other immune cell types.

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The Role of Monocytes and Macrophages in Autoimmune Diseases: A Comprehensive Review

Cited by 254 publications

References 364 publications

IKZF1 polymorphisms are associated with susceptibility, cytokine levels, and clinical features in systemic lupus erythematosus

IKZF1 polymorphisms are associated with susceptibility, cytokine levels, and clinical features in systemic lupus erythematosus

The impact of bariatric surgery on in-patient clinical outcomes among patients with autoimmune hepatitis

A quantitative model for the regulation of innate immune activation

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