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Immunodeficiency and Autoimmune Disorders
Research Guide

What is Immunodeficiency and Autoimmune Disorders?

Immunodeficiency and autoimmune disorders are conditions characterized by dysfunctions of the immune system, including deficiencies that increase susceptibility to infections and autoimmune responses where the immune system attacks the body's own tissues.

The field encompasses 99,017 published works examining mechanisms linking immune deficiencies to autoimmunity. Research highlights roles of T helper cell subsets like Th17 cells in driving pathogenic inflammation, as detailed in foundational studies on IL-17 and IL-23 pathways. Clinical advancements include therapies like infliximab for maintaining remission in Crohn's disease and ulcerative colitis.

99.0K
Papers
N/A
5yr Growth
986.9K
Total Citations

Research Sub-Topics

Why It Matters

Immunodeficiency and autoimmune disorders impact treatment of inflammatory bowel diseases and primary immunodeficiencies, with specific therapies demonstrating measurable clinical benefits. In the ACCENT I trial, maintenance infliximab therapy resulted in higher rates of clinical remission in Crohn's disease patients compared to placebo (Hanauer et al., 2002, "Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial"). Similarly, infliximab induction and maintenance increased clinical response rates at weeks 8, 30, and 54 in moderate-to-severe ulcerative colitis (Rutgeerts et al., 2005, "Infliximab for Induction and Maintenance Therapy for Ulcerative Colitis"). Recent developments include FDA acceptance of supplemental NDA for leniolisib in children aged 4-11 with activated phosphoinositide 3-kinase delta syndrome (APDS), addressing a rare immunodeficiency, though a Complete Response Letter was later issued for Joenja (leniolisib). Gene therapy for SCID-X1 corrected immunodeficiency in 9 of 10 patients but led to LMO2-associated clonal T cell proliferation in two cases (Hacein-Bey-Abina et al., 2003, "LMO2-Associated Clonal T Cell Proliferation in Two Patients after Gene Therapy for SCID-X1"). These examples underscore targeted interventions improving survival and quality of life in specific disorders.

Reading Guide

Where to Start

"IL-17 and Th17 Cells" by Korn et al. (2009) provides an accessible review of T cell differentiation into IL-17-producing subsets, foundational for understanding autoimmune mechanisms cited across the field.

Key Papers Explained

Bettelli et al. (2006, "Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells") establishes Th17-Treg balance, extended by Korn et al. (2009, "IL-17 and Th17 Cells") reviewing cytokine profiles and Langrish et al. (2005, "IL-23 drives a pathogenic T cell population that induces autoimmune inflammation") showing IL-23's role. Veldhoen et al. (2006, "TGFβ in the Context of an Inflammatory Cytokine Milieu Supports De Novo Differentiation of IL-17-Producing T Cells") details TGFβ-driven differentiation. Clinical translation appears in Hanauer et al. (2002, "Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial") and Rutgeerts et al. (2005, "Infliximab for Induction and Maintenance Therapy for Ulcerative Colitis").

Paper Timeline

100%
graph LR P0["Immunobiology: the immune system...
1995 · 4.1K cites"] P1["A frameshift mutation in NOD2 as...
2001 · 5.0K cites"] P2["Maintenance infliximab for Crohn...
2002 · 4.1K cites"] P3["IL-23 drives a pathogenic T cell...
2005 · 4.0K cites"] P4["Infliximab for Induction and Mai...
2005 · 3.8K cites"] P5["Reciprocal developmental pathway...
2006 · 6.8K cites"] P6["IL-17 and Th17 Cells
2009 · 4.7K cites"] P0 --> P1 P1 --> P2 P2 --> P3 P3 --> P4 P4 --> P5 P5 --> P6 style P5 fill:#DC5238,stroke:#c4452e,stroke-width:2px
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Most-cited paper highlighted in red. Papers ordered chronologically.

Advanced Directions

Recent preprints explore immune-related actinopathies linking immunodeficiency, autoimmunity, and autoinflammation via actin cytoskeleton defects. Progress in primary immunodeficiencies highlights improved diagnosis and treatment of inborn errors of immunity with autoimmune manifestations. FDA reviews of leniolisib for pediatric APDS indicate ongoing refinements in immunodeficiency therapies.

Papers at a Glance

In the News

Code & Tools

Recent Preprints

Latest Developments

Recent developments in immunodeficiency and autoimmune disorders research include innovative treatments such as resetting 'rogue' immune cells to manage autoimmune diseases like rheumatoid arthritis, lupus, and multiple sclerosis (PBS News, published 11/13/2025), advancements in immunotherapy including CAR-T cell therapies showing promising remission results (Nature, published 11/26/2025), and ongoing clinical trials exploring targeted CAR-T approaches for refractory autoimmune conditions (Nature Medicine, published 09/24/2025; and Nature Medicine, published 01/07/2026). Additionally, Nobel laureates have identified immune regulation mechanisms, such as peripheral immune tolerance, which are fundamental to understanding and treating these disorders (NobelPrize.org, published 10/06/2025).

Frequently Asked Questions

What role do Th17 cells play in autoimmune disorders?

Th17 cells produce IL-17 and drive pathogenic inflammation in autoimmune diseases. Bettelli et al. (2006) showed reciprocal developmental pathways generate pathogenic effector Th17 and regulatory T cells. Korn et al. (2009) detailed how CD4+ T cells differentiate into IL-17-producing Th17 subsets with distinct effector functions.

How does IL-23 contribute to autoimmune inflammation?

IL-23 drives a pathogenic T cell population inducing autoimmune inflammation, distinct from IL-12's role in Th1 cells. Langrish et al. (2005) demonstrated IL-23, composed of p19 and p40 subunits, promotes this population. This pathway is central to disorders like those studied in Crohn's disease susceptibility.

What is the genetic link between NOD2 mutations and Crohn's disease?

A frameshift mutation in NOD2 associates with susceptibility to Crohn's disease. Ogura et al. (2001) identified this mutation in "A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease". It highlights genetic factors in immunodeficiency-related autoimmunity.

What risks arise from gene therapy in SCID-X1?

Gene therapy for SCID-X1 corrected γc deficiency in 9 of 10 patients but caused LMO2-associated clonal T cell proliferation in two. Hacein-Bey-Abina et al. (2003) reported this in "LMO2-Associated Clonal T Cell Proliferation in Two Patients after Gene Therapy for SCID-X1". It demonstrates both efficacy and leukemogenic risks.

How effective is infliximab in ulcerative colitis?

Infliximab at weeks 0, 2, 6, and every eight weeks increased clinical response rates at weeks 8, 30, and 54 versus placebo in moderate-to-severe ulcerative colitis. Rutgeerts et al. (2005) confirmed this in "Infliximab for Induction and Maintenance Therapy for Ulcerative Colitis". ClinicalTrials.gov numbers NCT00036439 and NCT00096655 support these findings.

What are key genomic predictors in chronic lymphocytic leukemia?

Genomic aberrations in chronic lymphocytic leukemia independently predict disease progression and survival. Döhner et al. (2000) established this in "Genomic Aberrations and Survival in Chronic Lymphocytic Leukemia". These inform risk-adapted treatment strategies.

Open Research Questions

  • ? How can the balance between pathogenic Th17 and regulatory T cells be therapeutically modulated to prevent autoimmune inflammation?
  • ? What mechanisms underlie NOD2 frameshift mutations leading to Crohn's disease susceptibility?
  • ? How does IL-23 specifically drive pathogenic T cells without promoting Th1 development?
  • ? What factors trigger LMO2-associated clonal proliferation following SCID-X1 gene therapy?
  • ? Which genomic aberrations most accurately predict survival in chronic lymphocytic leukemia?

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