The role of inflammation in autoimmune disease: a therapeutic target

Abstract

Autoimmune diseases (AIDs) are immune disorders whose incidence and prevalence are increasing year by year. AIDs are produced by the immune system’s misidentification of self-antigens, seemingly caused by excessive immune function, but in fact they are the result of reduced accuracy due to the decline in immune system function, which cannot clearly identify foreign invaders and self-antigens, thus issuing false attacks, and eventually leading to disease. The occurrence of AIDs is often accompanied by the emergence of inflammation, and inflammatory mediators (inflammatory factors, inflammasomes) play an important role in the pathogenesis of AIDs, which mediate the immune process by affecting innate cells (such as macrophages) and adaptive cells (such as T and B cells), and ultimately promote the occurrence of autoimmune responses, so targeting inflammatory mediators/pathways is one of emerging the treatment strategies of AIDs. This review will briefly describe the role of inflammation in the pathogenesis of different AIDs, and give a rough introduction to inhibitors targeting inflammatory factors, hoping to have reference significance for subsequent treatment options for AIDs.

Unveiling the concealed reactivity of masked diformylmethane with RAHB-assisted enamines leads to dissymmetric di-meta-substituted pyridines

“…In ammation, a crucial innate defense mechanism, safeguards the body against infections triggered by pathogens, allergens, and toxins, thereby contributing to overall homeostasis 34 . However, when in ammation becomes chronically abnormal, it poses a signi cant threat, causing severe tissue damage and contributing to various diseases such as sepsis 43 , neurodegenerative disorders 44 , autoimmune conditions 45 , and even certain cancers 46 . Consequently, the urgent need for effective anti-in ammatory agents with innovative mechanisms of action is evident.…”

Putting Functional Gastrointestinal Disorders within the Spectrum of Inflammatory Disorders Can Improve Classification and Diagnostics of These Disorders

“…It has been known for a long time that inflammation plays a significant role in the pathogenesis of some diseases which often show a strong genetic influence, including musculoskeletal rheumatic diseases, IBS, psoriasis, and systemic autoimmune diseases [ 9 , 10 ]. Historically, they have been divided into two categories, autoinflammatory and autoimmune diseases, based on the differences in the underlying immune mechanisms.…”

“…Autoinflammatory diseases are characterized by abnormal innate immune responses without high-titer autoantibodies or autoreactive T lymphocytes [ 11 ]. On the contrary, the hallmark of autoimmune diseases is a failure of the specific (adaptive) immune system to differentiate self-antigens from foreign antigens (self/nonself discrimination) [ 9 ]. However, a necessary precondition for the promotion of autoreactive T and B cells and the progression of tissue and organ damage, once the tolerance to autoantigens has been lost, is the activation and abnormal proliferation of innate immune cells, macrophages, neutrophils, and DCs, which are capable of secreting a large amount of different inflammatory mediators, such as TNF-α, interleukins (ILs), and interferons (IFNs).…”

“…The key step in this process is the establishment of the permanent imbalance between the regulatory T cells (Treg cells) and the effector T cells (Teff cells), which can develop under the long-term influence of environmental factors or immune disturbances caused by preexisted pathologies [ 9 , 12 , 13 ]. An important fact to know is that Treg cells show a high degree of plasticity under altering micro-environmental conditions [ 14 ].…”

“…Regardless of the type of the initial stimuli, inflammatory conditions can be established in the microenvironment which are necessary for Teff cell activation and can eventually lead to the loss of tolerance to autoantigens and the cooperation of the innate and adaptive (specific) immune responses in promoting tissue damage and remodeling [ 9 ]. Which type of immune response will dominate, either a type 1 (cell-mediated) immune response, which involves innate immune cells, like DCs, macrophages, natural killer (NK) cells, and T helper cells type 1 (Th1 cells), or a type 2 (humoral, antibody-mediated) immune response, which is characterized by the activation of Th2 and B cells, antibody production, and tissue infiltration by eosinophils and mast cells, will depend on the local cytokine milieu and an individual’s genetic makeup [ 11 , 12 ].…”