Autoimmune Hemolytic Anemia

Autoimmune Hemolytic Anemia

Autoimmune hemolytic anemia (AIHA) is a complex autoimmune disorder characterized by the destruction of red blood cells (RBCs) by the immune system. As a leading company in the field, we are dedicated to providing innovative drug and therapy development services to address the challenges associated with AIHA.

Introduction to Autoimmune Hemolytic Anemia

Autoimmune Hemolytic Anemia is a condition where the body's immune system mistakenly identifies its own red blood cells as foreign and targets them for destruction. This immune response leads to a decrease in the number of circulating RBCs, resulting in anemia. AIHA can be classified into warm AIHA, where autoantibodies attack RBCs at body temperature, and cold AIHA, where autoantibodies target RBCs at colder temperatures.

  • Pathogenesis of Autoimmune Hemolytic Anemia
    The pathogenesis of AIHA involves the production of autoantibodies, predominantly IgG or IgM, which bind to antigens on the surface of RBCs. These autoantibodies can activate the complement system, leading to the destruction of RBCs through phagocytosis or complement-mediated lysis. In warm AIHA, the destruction primarily occurs in the spleen, where macrophages recognize and clear the antibody-coated RBCs. In cold AIHA, the autoantibodies cause RBC agglutination, triggering complement activation and subsequent hemolysis mainly in the peripheral circulation.

The relationship between autoimmune hemolytic anemia (AIHA) and infections during the course of the disease.Fig.1 The relationship between AIHA and infection. (Giannotta J. A., et al., 2021)

Drug Discovery and Development for Autoimmune Hemolytic Anemia

Monoclonal antibodies that target CD38 on plasma cells have shown efficacy in AIHA. These antibodies facilitate the depletion of plasma cells responsible for autoantibody production, leading to improved outcomes in cases with refractory AIHA. Moreover, corticosteroids, such as prednisone, are commonly used as first-line therapeutics to suppress immune activity and reduce autoantibody production. In more severe cases or cases resistant to corticosteroids, additional immunosuppressive agents like rituximab, cyclophosphamide, or azathioprine may be employed to control the autoimmune response.

Our company has a diversified therapy development platform, including targeted therapies and immunotherapies mentioned in the appeal. If you want to know more, please click on the link below.

Our Services

Autoimmune hemolytic anemia presents significant challenges in diagnosis and therapeutics, requiring innovative drug and therapy development services. Our company is committed to advancing the understanding and therapy development of AIHA through our comprehensive diagnostics, animal model development, and preclinical research services. By leveraging targeted therapies and immunosuppressive approaches, we strive to provide effective therapy for AIHA.

Animal Models

  • Primary AIHA Murine Model Development
    One of our notable contributions is the development of a murine model using HOD and OTII mice. By selectively breeding these strains, we have successfully generated offspring with both autoimmune (HOD+OTII+) and non-autoimmune (HOD-OTII+) genotypes. This model allows for the study of the establishment of tolerance to RBC autoantigens and the progression of autoimmune responses against RBCs.
  • Levodopa-Induced AIHA Model Development
    One of our successful induced disease models involves the administration of levodopa, a medication used in human therapy, to C57BL/6 mice. By multiple injections or oral feeding of levodopa, we induced cycles of IgM, IgG, and IgA autoantibody responses against mouse red blood cells (RBCs). Levodopa injection primarily induced IgM and IgG autoantibodies, while levodopa feeding enhanced the production of IgA autoantibodies.
  • Transgenic Model Development
    We developed a double transgenic mouse model bearing immunoglobulin heavy and light chain genes encoding an autoantibody against mouse erythrocytes. By crossing C57BL/6 mice carrying the transgene for each chain of the immunoglobulin, we successfully generated mice in which most B cells expressed the autoantibody on their surface.

In Vitro Models

  • Primary Cell Culture
    In AIHA, autoantibodies target and destroy red blood cells. To mimic this process, we have successfully developed primary cell culture models using patient-derived peripheral blood mononuclear cells (PBMCs) and red blood cells (RBCs). By isolating PBMCs from AIHA patients and co-culturing them with RBCs, we can observe the interactions between autoantibodies and RBCs, leading to hemolysis.
  • Immortalized Cell Lines
    One of our notable contributions is the development of an immortalized B-cell line expressing autoantibodies against RBCs. By transfecting a B-cell line with the genes encoding these autoantibodies, we have successfully established a cell line that produces and secretes autoantibodies specific to RBC antigens.

Our Advantages

Time-saving services with high efficiency

Fast and cost-efficient workflow

Timely project reporting and after-sales service

Professional and experienced multidisciplinary experts

Careful design and transparent operation process

Superior data quality and fast turnaround

Our experienced team of scientists and researchers utilize state-of-the-art technologies and methodologies to evaluate the pharmacokinetics, safety, efficacy, and mechanism of action of potential therapeutics in AIHA models. In addition to the services and models listed above, we also provide customized services and disease model development services to meet your specific needs. If you are interested in our services, please don't hesitate to contact us.

References

  1. Giannotta J. A., et al. "Infectious complications in autoimmune hemolytic anemia." Journal of Clinical Medicine 10.1 (2021): 164.
  2. Xiao Z., and Murakhovskaya, I. "Development of new drugs for autoimmune hemolytic anemia." Pharmaceutics 14.5 (2022): 1035.
For research use only. Not intended for any clinical use.