Request Demo

Last update 08 May 2025

IL-12Rβ2

Last update 08 May 2025

Basic Info

Synonyms

IL-12 receptor subunit beta-2, IL-12R subunit beta-2, IL-12R-beta-2

+ [5]

Introduction

Receptor for interleukin-12. This subunit is the signaling component coupling to the JAK2/STAT4 pathway. Promotes the proliferation of T-cells as well as NK cells. Induces the promotion of T-cells towards the Th1 phenotype by strongly enhancing IFN-gamma production.

Drugs associated with IL-12Rβ2

WO2024018241

Patent Mining

Target

IL-12Rβ2

Mechanism-

Active Org.

Ghent University [+2]

Originator Org.

dualyx NV [+2]

Active Indication

Eye Diseases [+3]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2024018242

Patent Mining

Target

IL-12Rβ2

Mechanism-

Active Org.

dualyx NV [+2]

Originator Org.

dualyx NV [+2]

Active Indication

Immune System Diseases [+3]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with IL-12Rβ2

100 Translational Medicine associated with IL-12Rβ2

0 Patents (Medical) associated with IL-12Rβ2

461

Literatures (Medical) associated with IL-12Rβ2

01 Jul 2025·Journal of Neuroimmunology

Autoantigen and IL-2 activated CD4+CD25+T regulatory cells are induced to express CD8 and are autoantigen specific in inhibiting experimental autoimmune encephalomyelitis

Article

Author: Robinson, Catherine M ; Rakesh, Prateek ; Verma, Nirupama D ; Hall, Bruce M ; Tran, Giang T ; Hodgkinson, Suzanne J ; Bedi, Sukhandep ; Carter, Nicole ; Al-Atiyah, Ranje

Experimental autoimmune encephalomyelitis (EAE) induced by immunization with myelin basic protein (MBP) is a self-limiting disease model of multiple sclerosis. CD4⁺CD25⁺Foxp3⁺T cells play a role in limiting autoimmune disease but treatment with antigen naïve CD4⁺CD25⁺ cells does not reduce EAE. This study examined if in vitro activation by MBP and rIL-2 induced CD4⁺CD25⁺Foxp3⁺ cells that could inhibit EAE. Culture of CD4⁺CD8^-CD25⁺cells from naïve rats with MBP and rIL-2 induced activated Treg that reduced the severity of clinical EAE and infiltration of CD8⁺T cells and macrophage into brain stem. CD4⁺CD25⁺T cells activated by an irrelevant autoantigen and rIL-2 did not suppress EAE. Resting CD4⁺CD25⁺T cells activated by autoantigen and rIL-2 have mRNA for Infgr, Il12rb2, Il5 but not Tbet, Gata3, Ilr5ra or Ifng. These changes in mRNA expression are the markers of Ts1 cells. A proportion of CD4⁺CD8^-CD25⁺ cells activated by MBP/rIL-2 were induced to express CD8α, CD8β and CD62L. Depletion of CD4⁺CD8α⁺CD25⁺ cells removed the capacity of MBP and rIL-2 activated CD4⁺CD25⁺T cells to suppress EAE. This study demonstrated that in vitro activation of CD4⁺CD8^-CD25⁺ cells by MBP/rIL-2 induced relevant antigen-specific Treg within days, which expressed CD8α, CD8β and CD62L with a Ts1 phenotype and that had greater potency than freshly isolated antigen naive CD4⁺CD25⁺Treg in suppressing clinical severity of EAE and immune inflammation in CNS. These findings may guide development of antigen-specific Treg for therapy.

01 Apr 2025·Mucosal Immunology

Gut-homing and intestinal TIGITnegCD38+ memory T cells acquire an IL-12-induced, ex-Th17 pathogenic phenotype in a subgroup of Crohn’s disease patients with a severe disease course

Article

Author: Escher, Johanna C ; Joosse, Maria E ; Costes, Léa M M ; Kemos, Polychronis ; Hulleman-van Haaften, Danielle H. ; Calado, Beatriz ; Hulleman-van Haaften, Daniëlle H ; Ruemmele, Frank M ; Aardoom, Martine A. ; Samsom, Janneke N. ; Tuk, Bastiaan ; Joosse, Maria E. ; de Ridder, Lissy ; Tindemans, Irma ; Barendregt, Daniëlle M H ; Samsom, Janneke N ; Croft, Nicholas M ; Escher, Johanna C. ; van Berkel, Lisette A ; Costes, Lea M.M. ; Klomberg, Renz C W ; van Berkel, Lisette A. ; Aardoom, Martine A ; Klomberg, Renz C.W. ; Croft, Nicholas M. ; Heredia, Maud ; Ruemmele, Frank M. ; Barendregt, Danielle M.H.

CD4⁺ memory T cell (T_M) reactivation drives chronicity in inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis. Defects driving loss of T_M regulation likely differ between patients but remain undefined. In health, approximately 40 % of circulating gut-homing CD38⁺T_M express co-inhibitory receptor T-cell immunoreceptor with immunoglobulin and ITIM domains (TIGIT). TIGIT⁺CD38⁺T_M have regulatory function while TIGIT^negCD38⁺T_M are enriched in IFN-γ-producing cells. We hypothesized TIGIT^negCD38⁺T_M are inflammatory and drive disease in a subgroup of IBD patients. We characterized TIGIT⁺CD38⁺T_M in a uniquely large cohort of pediatric IBD patients from time of diagnosis into adulthood. Circulating TIGIT^negCD38⁺T_M frequencies were higher in a subgroup of therapy-naïve CD patients with high plasma IFN-γ and a more severe disease course. TIGIT^negCD38⁺T_M were highly enriched in HLA-DR⁺ and ex-Th17/Th1-like cells, high producers of IFN-γ. Cultures of healthy-adult-stimulated T_M identified IL-12 as the only IBD-related inflammatory cytokine to drive the pathogenic ex-Th17-TIGIT^negCD38⁺ phenotype. Moreover, IL12RB2 mRNA expression was higher in TIGIT^negCD38⁺T_M than TIGIT⁺CD38⁺T_M, elevated in CD biopsies compared to controls, and correlated with severity of intestinal inflammation. Overall, we argue that in a subgroup of pediatric CD, increased IL-12 signaling drives reprogramming of Th17 to inflammatory Th1-like TIGIT^negCD38⁺T_M and causes more severe disease.

01 Apr 2025·Rheumatology

Association between interleukin-12 p40 subunit and risk of primary Sjögren’s disease: a Mendelian randomization study

Article

Author: Yang, Zijing ; Wincup, Chris ; Galloway, James B ; Warwick, Alasdair ; Russell, Mark D ; Zuckerman, Benjamin P ; Zhao, Sizheng Steven

AbstractObjectivesIL-12 signalling was proposed in the immunopathogenesis of primary Sjögren’s disease. The efficacy of therapies targeting this pathway is currently unclear. Herein, we investigated the associations between circulating proteins involved in the IL-12 and IL-23 signalling pathways on primary Sjögren’s disease using Mendelian randomization.MethodsWe selected single nucleotide polymorphisms from protein quantitative trait loci of IL12A, IL12B, IL12Rβ1, IL12Rβ2 and IL23R to examine the association between alterations in their levels and risk of primary Sjögren’s disease. Genetic association data for proteins were taken from studies ranging from 3301 to 54 306 in sample size, and from 3232 cases of primary Sjögren’s disease and 17 481 controls. The Wald ratio or inverse variance weighted methods estimated causal effects. We applied colocalization and pleiotropy-robust methods as sensitivity analyses for confounding.ResultsThere was a negative association between genetically predicted IL-12p40 (encoded by IL12B) and primary Sjögren’s disease. In the two independent exposure datasets odds ratio (OR), 0.79 (95% CI 0.68–0.93; P-value = 0.004) and OR 0.86 (95% CI 0.78–0.95; P-value = 0.003) per S.D. decrease in genetically predicted IL-12p40. Neither IL-12Rβ2 nor IL-23R met the threshold P-value after Mendelian randomization analyses (P-value < 0.01) for colocalization assessment. No variants for the IL12A gene met prerequisite thresholds for weak instrument bias.ConclusionThis study provides genetic evidence that IL-12p40 has a causal role in primary Sjögren’s disease pathogenesis. Our data suggest that decreasing levels of IL-12p40 may be deleterious. We would not suggest selecting this drug target as a therapeutic option.

Analysis

Perform a panoramic analysis of this field.

view full example data

Hiro LS Researcher

The AI Search Engine Built to Accelerate Biopharma Decisions

Search across billion-scale life sciences data to uncover signals, validate evidence, and act with confidence.

Ask any biopharma research question→

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, Patsnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Discover Synapse Data Servers

Synapse data is now integrated into the PatSnap LS Model Context Protocol (MCP) service. Customize your LLM agent now using our MCP server!

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

IL-12Rβ2

Basic Info

Related

Analysis