To target the pathogenesis of diseases, innate or adaptive immune system, numerous biological drugs have been approved, targeting multiple mechanisms of the immune and inflammatory cascade.1


Xiao Q, et al. Biological drug and drug delivery-mediated immunotherapy. Acta Pharmaceutica Sinica B 2021;11(4):941-960

Immunology biosimilars

Biologic agents have become indispensable in the management of autoimmune diseases. The introduction of biosimilars into the market has helped increase competition allowing costs to be reduced while maintaining efficacy.1


Rischin A and Östör AJK. Update on biosimilars in rheumatology. Inflammopharmacology 2017;25(2):177-184.

Immunology biosimilars (extended)

Immune-mediated inflammatory diseases (IMIDs) are debilitating progressive diseases that require timely intervention and continuous management. 

The therapeutic aims for all IMIDs are identical: to gain rapid control of inflammation, prevent tissue damage, improve QoL and, if possible, achieve long‐term disease remission. In achieving these aims, targeted biologic therapy has been revolutionary.2 The timing of therapy is paramount and treatment should commence early for optimal outcome.2

However, current guidelines often reserve these drugs for patients with more severe disease and/or patients who have failed to respond to multiple other treatments.1 In some countries, access to biologics may then be further limited by the implementation of national eligibility and reimbursement criteria,1 creating a high unmet need in many countries worldwide.


  1. Edwards CJ, Hercegová J, et al. Switching to biosimilars: current perspectives in immune-mediated inflammatory diseases. Expert Opinion on Biological Therapy 2019; 19(10):1001-1014
  2. Keuk A, Hazleman BL, et al. Immune‐mediated inflammatory diseases (IMIDs) and biologic therapy: a medical revolution. Postgrad Med 2007; 83(978): 251–260.

Mechanisms of IMIDs1,2

IMID, immune-mediated inflammatory disease.



  1. Ermann J and Fathman CG. Autoimmune diseases: genes, bugs and failed regulation. Nat Immunol 2001;2:759–761
  2. Adapted from Rosenblum MD, Remedios KA, et al. Mechanisms of human autoimmunity. J Clin Invest 2015;125:2228–2233

Each IMID has a specific pathway:

APC, antigen-presenting cell; AS, ankylosing spondylitis; CD, Crohn’s disease; IFN, interferon; IL, interleukin; PsA, psoriatic arthritis; Pso, psoriasis; RA, rheumatoid arthritis; TGF, transforming growth factor; TNF, tumour necrosis factor; UC, ulcerative colitis.


  1. Adapted from Coates LC, FitzGerald O, et al. Psoriasis, psoriatic arthritis, and rheumatoid arthritis: Is all inflammation the same? Semin Arthritis Rheum 2016;46:291–304;
  2. Abraham C and Cho JH. Inflammatory bowel disease. N Engl J Med 2009;361:2066–2078;
  3. Brand S. Crohn's disease: Th1, Th17 or both? The change of a paradigm: new immunological and genetic insights implicate Th17 cells in the pathogenesis of Crohn's disease. Gut 2009;58:1152–1167;
  4. Heller F, Fuss IJ, et al. Oxazolone colitis, a Th2 colitis model resembling ulcerative colitis, is mediated by IL-13-producing NK-T cells. Immunity 2002;17:629–638;
  5. Weigmann B and Neurath MF. IL-9 and Th9 cells in health and diseases—from tolerance to immunopathology. Semin Immunopathol 2017;39:89–95;
  6. Smith JA and Colbert RA. Review: The interleukin-23/interleukin-17 axis in spondyloarthritis pathogenesis: Th17 and beyond. Arthritis Rheumatol 2014; 66:231–241;
  7. Taams LS, Palmer DB, et al. Regulatory T cells in human disease and their potential for therapeutic manipulation. Immunology 2006;118:1–9.