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Antigen Processing Pathways01:31

Antigen Processing Pathways

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MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
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Antigens Involved in Adaptive Immunity01:26

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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
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Diabetes Mellitus: Overview and Type I Subtype01:22

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Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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Pathophysiology of Diabetes01:20

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Antigen Presenting Cells01:22

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The immune system is a complex network of cells and molecules that protects the body from foreign invaders. T cells, a type of white blood cell, play a crucial role in this process. They recognize and attack foreign substances, such as pathogens, that enter the body.
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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
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The MHC Class II Antigen-Processing and Presentation Pathway Is Dysregulated in Type 1 Diabetes.

Ambroise Gilles1, Lan Hu2, Francesca Virdis3

  • 1Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ.

Journal of Immunology (Baltimore, Md. : 1950)
|October 9, 2023
PubMed
Summary

Type 1 diabetes (T1D) disrupts the MHC class II (MHCII) antigen processing pathway, showing increased MHCII-CLIP levels and altered HLA-DM (DM) and HLA-DO (DO) expression in immune cells, indicating a significant pathway dysregulation in T1D patients.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Endocrinology

Background:

  • Peptide loading onto MHC class II (MHCII) molecules is crucial for immune response and is regulated by HLA-DM (DM) and HLA-DO (DO).
  • MHCII-peptide presentation is abnormal in type 1 diabetes (T1D), contributing to immune tolerance breakdown.
  • Previous studies lacked direct measurements of MHCII pathway activity in T1D patients.

Purpose of the Study:

  • To directly measure and analyze the activity of the MHCII antigen-processing pathway in T1D patients.
  • To investigate the levels of MHCII, MHCII-CLIP, DM, and DO in immune cells of T1D patients and healthy controls.

Main Methods:

  • Flow cytometry was used to quantify MHCII, MHCII-CLIP, DM, and DO levels in peripheral blood B cells, dendritic cells, and monocytes.
  • Gene expression profiling of peripheral blood mononuclear cell (PBMC) RNA was performed.
  • Analysis included 99 T1D patients and 97 healthy controls.

Main Results:

  • MHCII levels were comparable between T1D patients and controls across all analyzed cell types.
  • MHCII-CLIP levels were significantly elevated (up to 3.4-fold in B cells) in all APC subsets of T1D patients.
  • DM and DO levels were unexpectedly similar in T1D patients and controls, despite increased MHCII-CLIP.
  • Elevated DMB mRNA in T1D patients with residual C-peptide correlated with increased DM protein in B cells and dendritic cells.
  • Increased DO levels were also observed in T1D patients with residual C-peptide.

Conclusions:

  • The MHCII antigen-processing pathway is significantly dysregulated in T1D patients.
  • Elevated MHCII-CLIP levels suggest impaired CLIP release or MHCII stabilization.
  • Differential regulation of the MHCII pathway may be associated with residual C-peptide levels in T1D individuals.