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Immune System Models

Autoimmune Mouse Model

Since 1998, ingenious targeting laboratory has supported autoimmune disease research with custom mouse models enabling mechanistic studies of immune tolerance breakdown, autoreactive lymphocyte development, and therapeutic interventions targeting aberrant immune responses.

Autoimmune disease mouse models provide essential platforms for investigating the molecular pathways underlying loss of self tolerance, testing hypotheses about genetic susceptibility, and developing therapies for conditions including lupus, rheumatoid arthritis, multiple sclerosis, and type 1 diabetes.

2,500+
Projects Completed
800+
Publications
26+
Years Experience
100%
Success Rate

Categories of Autoimmune Disease

Autoimmune diseases arise when the immune system fails to distinguish self from non self, leading to attack on the body's own tissues. Mouse models enable controlled study of specific genetic contributions to immune tolerance and autoreactivity.

Systemic Autoimmunity

Diseases affecting multiple organ systems, including systemic lupus erythematosus (SLE), rheumatoid arthritis, and Sjogren syndrome.

Organ Specific Autoimmunity

Diseases targeting specific tissues, including type 1 diabetes (pancreas), multiple sclerosis (nervous system), and autoimmune thyroiditis.

Inflammatory Bowel Disease

Immune mediated intestinal inflammation including Crohn disease and ulcerative colitis.

Spontaneous Autoimmune Models

MRL/lpr

Mice homozygous for the lpr mutation in Fas develop severe lupus with lymphadenopathy, autoantibodies, and glomerulonephritis.

NZB/W F1

Hybrid offspring of NZB and NZW strains develop lupus like disease with anti DNA antibodies and nephritis. Female predominance mirrors human SLE.

NOD (Non Obese Diabetic)

Spontaneous development of autoimmune diabetes with insulitis and beta cell destruction. Widely used for T1D research.

K/BxN

T cell receptor transgenic model developing severe inflammatory arthritis. Serum transfer induces arthritis in naive recipients.

Key Pathways in Autoimmunity

Interferon Signaling

  • IFNAR Knockout: Interferon alpha/beta receptor knockout protects from lupus
  • STING Pathway: Links DNA sensing to type I interferon production
  • IRF Family: Controls interferon gene expression

B Cell Tolerance

  • BCR Signaling: Modulation affects autoreactive B cell fate
  • BAFF/APRIL: B cell survival factors influence persistence
  • TLR Signaling: Intrinsic TLR7 and TLR9 promote activation

T Cell Tolerance

  • Central Tolerance: Aire controls tissue restricted antigen expression
  • Peripheral Tolerance: Regulatory T cells maintain tolerance
  • Th17 Cells: IL17 producing T helper cells drive inflammation

Conditional Approaches

Tissue or cell type specific gene deletion enables dissection of contributions from different immune cell populations.

T Cell Specific

CD4 Cre or Lck Cre

Reveals T cell intrinsic requirements for tolerance

B Cell Specific

CD19 Cre or Mb1 Cre

Targets B lymphocytes for autoantibody studies

Dendritic Cell Specific

CD11c Cre

Examines antigen presenting cell contributions

Tissue Specific

Organ specific Cre

Target organ specific gene deletion for organ specific autoimmunity

Phenotyping Autoimmune Models

Serological Assessment

  • Autoantibodies: ELISA for anti nuclear, anti dsDNA, rheumatoid factor
  • Immunoglobulin levels: Total IgG, IgM, IgA quantification
  • Inflammatory markers: Cytokines, chemokines, complement

Organ Assessment

  • Kidney: Proteinuria, BUN, creatinine for lupus nephritis
  • Joints: Clinical scoring, histology for synovitis and erosion
  • CNS: Clinical scoring for EAE, demyelination histology

Immune Cell Analysis

  • Flow cytometry: Lymphocyte populations, activation markers, Tregs
  • Tissue infiltration: Immunohistochemistry for immune cells
  • Functional assays: Proliferation, cytokine production

Selected Publications in Autoimmune Research

Recent publications demonstrate the utility of genetically engineered mouse models in autoimmune disease research:

What Researchers Say

I've been working with iTL over the past 5 years in the production of 3 different genetically altered mice. Not only did iTL help in the design of the mice, but the entire process was transparent with the opportunity at any time along the way to discuss my questions or concerns with scientists who had significant insight into the process. The mice were delivered on time, as billed!

Raghu Mirmira, MD, PhD

University of Chicago

Start Your Autoimmune Model Project

Our scientific consultants are ready to discuss your autoimmune research requirements and recommend the optimal model design for your program. Initial consultation is provided at no charge.

✦ New for 2026

Breeding Scheme Architect

Plan complex multi-allele breeding strategies, calculate expected genotype ratios, and estimate time to experimental cohorts—all before starting your project.

Visualize multi-generation breeding paths
Calculate Mendelian ratios automatically
Estimate timeline to study-ready cohorts

Free Research Tool

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Allele 1Gene-flox (conditional)
Allele 2Cre-driver (tissue-specific)
TargetHomozygous knockout

→ 3 generations to target genotype

Frequently Asked Questions

C57BL/6 is relatively resistant to many autoimmune conditions and is well characterized for immune studies. BALB/c has different immune response profiles (Th2 biased). Autoimmune prone backgrounds like MRL, NZB/W, and NOD carry multiple susceptibility alleles and may be appropriate for specific disease models.

Yes. Conditional knockouts are valuable for autoimmune research to achieve cell type specific deletion (e.g., T cell, B cell, or myeloid specific) and to avoid developmental effects. Tamoxifen inducible deletion in adults prevents developmental compensation and better models therapeutic intervention.

Important pathways include interferon signaling (IFNAR, STING, IRF family), B cell tolerance (BCR signaling, BAFF/APRIL, TLR signaling), T cell tolerance (central and peripheral tolerance, regulatory T cells, Th17 cells), and myeloid cell contributions (neutrophils, macrophages, dendritic cells).

Standard assessments include autoantibody titers (ELISA, immunofluorescence), immune cell analysis (flow cytometry for T cells, B cells, myeloid cells), histopathology (organ specific inflammation and damage), cytokine profiling, and functional assays (T cell proliferation, B cell activation).

Lab Signals

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