not-yet-known not-yet-known not-yet-known unknown Introduction: Myasthenia gravis (MG) is primarily caused by autoantibodies that have detrimental effects on neuromuscular junctions. There are two subtypes of MG, namely generalized MG (GMG) and ocular MG (OMG). Half of the patients with MG have OMG, and more than half of the patients with OMG could progress to having GMG in 2 years. Neurologists are mostly concerned about the possibility of the occurrence of OMG and when it would transition to GMG. Now, there have been numerous studies on experimental autoimmune myasthenia gravis (EAMG) for GMG; however, there have been very few available studies on OMG EAMG, which were focused on anti-muscle nicotinic acetylcholine receptor and involved using the GMG EAMG protocol. Result and Discussion: We summarize the literature on the clinical and basic information in OMG, focusing on their related autoantibodies, conversion, treatment dilemmas, and animal models and the gene, protein, function, and EAMG of low-density lipoprotein receptor-related protein 4 (LRP4). LRP4 is a key protein in the neuromuscular junction. Based on the above evidence, a strong relationship was observed between OMG and LR4, suggesting that the LRP4 EAMG might be a good candidate to mimic OMG.

The success efficacy of B cell clearance depletion therapy in multiple sclerosis (MS) highly suggests strongly indicates the role involvement of B cells in the pathogenesis of MSdisease’s pathogenesis, posing thereby presenting a serious significant challenge to the existing classical pathogenesis conventional understanding of MS (i.e. T cell-mediated autoimmune diseases). pathogenesis.Both of CXCR5+CD8++ T cells [(follicular cytotoxic T cells, Tfc) and CXCR5+CD4+ T cells (follicular helper T cells, Tfh) serve as pivotal immune cells that bridge B cell and T cell interactions. While Tfc cells significantly contribute to the development of tumors and viral infections, they have been infrequently documented in autoimmune diseases, particularly in MS. CXCL13/CXCR5 is an important signaling pathway in Tfc cells, closely related to various cellular events.Evidence indicates that the pathway involving CXCR5 dysregulation is linked to tumor development and viral infections; however, the CXCL13/CXCR5 axis signaling pathway has seldom been documented in autoimmune diseases, especially in multiple sclerosis. In current review, we summaried current publications from pubmed including Tfc, CXCL13/CXCR5 axis and autoimmune diseases, tried to final the best protocol to study the role of Tfc in MS.

Amyloid beta plaques and tau tangles are the primary hallmarks of Alzheimer’s disease (AD). Recently, marked advances have been made in terms of passive anti-Aβ immunotherapy for AD, which have been supported by evidence from AD animal models and clinical trials. While innate immunity significantly contributes to the pathology of AD, it does not fully clarify the immune mechanisms linked to its pathogenesis. Consequently, focus should be directed toward adaptive immunity, encompassing both humoral immunity, primarily governed by B cells, and cellular immunity, predominantly influenced by T cells. T cells, in particular, may also be important in AD pathogenesis, as indicated by many lines of evidence from clinical and animal studies. Furthermore, T cells that infiltrate the central nervous system (CNS) have demonstrated both protective and detrimental effects on neural tissue in AD. Because autoreactive CD8+ T cells were expected to be cytotoxic to CNS cells, they have received less attention. Nevertheless, a significant amount of evidence now suggests that CD8+ Treg cells play a role in multiple diseases. However, the function of anti-Aβ-specific CD8+ T cells in AD has remained ambiguous. Many subsets of CD8+ T cells exist, which have been well-studied in terms of autoimmunity. We suggest that these CD8+ T cell subsets identified in AD studies could constitute a promising area for future AD research.

：Parkinson’s disease (PD) is a relatively common neurodegenerative disorder of the nervous system, mainly characterized by motor disorders and non-motor symptoms. Although the specific causes of this disease have not been fully clarified yet, significant progress has been made in the research on its pathological mechanism. Currently, while there is no cure, drug development has made notable advancements in symptom relief and short-term improvement. In recent years, immunotherapy has shown great potential in PD treatment, with vaccines and monoclonal antibodies targeting α-synuclein（a-syn） being actively developed. Early identification of non-motor symptoms in PD is crucial for timely intervention and disease management. Research indicates that immune system abnormalities, including autoimmunity and activation of both central and peripheral immune systems, play a significant role in the development of PD. Currently, various immunotherapy strategies are in clinical trials, such as active and passive immunotherapies, aiming to clear or prevent the aggregation of harmful proteins and thereby slow disease progression. This article reviews the progress of immunotherapy in PD patients, explores the impact of non-motor symptoms and treatment strategies, and summarizes the development of new drugs in clinical trials. By reviewing existing literature, this article aims to provide new ideas and methods for the future drug treatment of PD.

not-yet-known not-yet-known not-yet-known unknown Chimeric Antigen Receptor T-cell (CAR-T) therapy, an innovative method in cancer immunotherapy, has shown remarkable effectiveness in addressing several hematological malignancies. Recent developments in immunology indicate that CAR-T therapy could potentially be applicable to treating autoimmune conditions, including rheumatoid arthritis, systemic lupus erythematosus, and type 1 diabetes. This review aims to explore the mechanisms underlying CAR-T therapy in both cancer and autoimmune diseases, highlighting the similarities and differences in its therapeutic targets and immune modulation strategies.The therapy mainly operates by genetically altering T cells to recognize and target specific antigens present on cancer cells or dysfunctional immune cells associated with autoimmune reactions. In autoimmune diseases, CAR-T can be designed to target pathogenic B cells, T cells, or other immune cell populations responsible for tissue damage. While the application of CAR-T in autoimmune diseases remains largely experimental, early clinical studies show promising results, though challenges such as immune tolerance, cytokine release syndrome, and neurotoxicity remain.Furthermore, this review examines the latest advancements and clinical implementations of CAR-T therapy in treating autoimmune disorders of the nervous system, such as Myasthenia Gravis, Neuromyelitis Optica Spectrum Disorder, Guillain-Barré Syndrome, Idiopathic Inflammatory Myopathy, Multiple Sclerosis, Autoimmune Encephalitis, and Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease. Despite being in its early stages, CAR-T therapy presents a novel and highly promising strategy for modulating the immune system in autoimmune diseases, with the potential to reshape therapeutic paradigms in the future.