Sanofi US - Type 2 Inflammation

For US residents only

IL-4, IL-13, and IL-5
Are Key Mediators of
Type 2 Inflammation¹

The IL-4, IL-13, and IL-5 cytokine pathways act specifically within the Type 2 inflammatory cascade.^1,2 One or more of these signaling pathways contribute to disease-specific effects or to inflammatory effects found across different diseases.¹

Type 2 cytokine effects
across diseases^1,2,a

^aAdditional Type 2 inflammatory mediators include thymic stromal lymphopoietin (TSLP), IL-25, IL-31, and IL-33.^1,6

^bGroup 2 innate lymphoid cells (ILC2) are an alternate source of IL-13 and IL-5. In asthma and CRSwNP, but not in skin conditions, ILC2 is also a source of IL-4.^2,7

IL-4, IL-13, and IL-5 are
principal cytokines in these
3 prominent diseases^1,6

^aIL-5, while present, has not been found to be a driver of the key pathophysiologic effects of atopic dermatitis.⁶

CRSwNP=chronic rhinosinusitis with nasal polyposis; IgE=immunoglobulin E; IL=interleukin; Jak=Janus kinase; Th0=T helper cell 0; Th2=T helper cell 2.

References

Gandhi NA, Bennett BL, Graham NM, Pirozzi G, Stahl N, Yancopoulos GD. Targeting key proximal drivers of Type 2 inflammation in disease. Nat Rev Drug Discov. 2016;15(1):35-50.
Robinson D, Humbert M, Buhl R, et al. Revisiting Type 2-high and Type 2-low airway inflammation in asthma: current knowledge and therapeutic implications. Clin Exp Allergy. 2017;47(2):161-175.
Hönzke S, Wallmeyer L, Ostrowski A, et al. Influence of Th2 cytokines on the cornified envelope, tight junction proteins, and β-defensins in filaggrin-deficient skin equivalents. J Invest Dermatol. 2016;136(3):631-639.
Wise SK, Laury AM, Katz EH, Den Beste KA, Parkos CA, Nusrat A. IL-4 and IL-13 compromise the sinonasal epithelial barrier and perturb intercellular junction protein expression. Int Forum Allergy Rhinol. 2014;4(5):361-370.
Saatian B, Rezaee F, Desando S, et al. Interleukin-4 and interleukin-13 cause barrier dysfunction in human airway epithelial cells. Tissue Barriers. 2013;1(2):e24333. doi:10.4161/tisb.24333
Noda S, Krueger JG, Guttman-Yassky E. The translational revolution and use of biologics in patients with inflammatory skin diseases. J Allergy Clin Immunol. 2015;135(2):324-336.
Boonpiyathad T, Sözener ZC, Satitsuksanoa P, Akdis CA. Immunologic mechanisms in asthma. Semin Immunol. 2019;46:101333. doi:10.1016/j.smim.2019.101333

IMM.20.10.0003 Last Update: [12/20]

More to Know

Disease Drivers

IL-4, IL-13, and IL-5
Are Key Mediators of
Type 2 Inflammation¹

Type 2 cytokine effects
across diseases^1,2,a

IL-4, IL-13, and IL-5 are
principal cytokines in these
3 prominent diseases^1,6

Type 2 Cytokines in
Different Diseases

Jak Enzymes and Cytokines

Barrier Dysfunction in
Different Diseases

Questions or Comments?

References

More to Know

Disease Drivers

IL-4, IL-13, and IL-5 Are Key Mediators of Type 2 Inflammation1

Type 2 cytokine effects across diseases1,2,a

IL-4, IL-13, and IL-5 are principal cytokines in these 3 prominent diseases1,6

Type 2 Cytokines in Different Diseases

Jak Enzymes and Cytokines

Barrier Dysfunction in Different Diseases

Questions or Comments?

References

IL-4, IL-13, and IL-5
Are Key Mediators of
Type 2 Inflammation¹

Type 2 cytokine effects
across diseases^1,2,a

IL-4, IL-13, and IL-5 are
principal cytokines in these
3 prominent diseases^1,6

Type 2 Cytokines in
Different Diseases

Barrier Dysfunction in
Different Diseases