Chauhan P, Hu S, Sheng WS, Prasad S, Lokensgard JR (2025) bTRM control of murine cytomegalovirus cns reactivation. 26(11):5275. doi: 10.3390/ijms26115275 PMID: 40508083

Objective: To determine the role of CD8+ and CD103+ brain-resident memory T cells (bTRMs) in controlling murine cytomegalovirus (MCMV) reactivation in the central nervous system.

Summary: Depleting CD103+ bTRMs led to transient viral gene expression and delayed recovery of infectious virus from explants, implicating these cells in maintaining latency. bTRM depletion also triggered expression of disease-associated microglial genes, suggesting a role in modulating neuroimmune responses.

Usage: Anti-CD103-SAP (IT-50) was injected intracerebroventricularly (2 µg) to selectively deplete CD103+ bTRMs in latently infected mice. This targeted depletion achieved ~90% T-cell reduction and was critical for assessing viral reactivation and microglial activation phenotypes.

Related Products: Anti-CD103-SAP (Cat. #IT-50)

Saavedra FM, Brotto DB, Joag V, Matson CA, Nesmiyanov PP, Herzberg MC, Vezys V, Masopust D, Stolley JM (2025) Triggering mouth-resident antiviral CD8+ T cells potentiates experimental periodontitis. Mucosal Immunol S1933-0219(25)00021-2. doi: 10.1016/j.mucimm.2025.02.003 PMID: 39988203

Objective: To determine if local reactivation of antigen-specific oral CD8+ TRM exacerbates ligature-induced periodontitis (LIP) in mice.

Summary: Topical application of virus-mimicking peptides during LIP increased alveolar bone loss, enhanced gingival and cervical lymph node inflammation, and upregulated gingival genes linked to innate immunity and cytotoxicity. Depleting CD103+ CD8+ TRM with αCD103-SAP prior to LIP prevented disease exacerbation, implicating these cells in periodontitis pathology.

Usage: Anti-CD103-SAP (IT-50) was administered in PBS at 5 μg (day -4), 2 μg (day 0), and 2 μg (day +4) relative to LIP induction.

Related Products: Anti-CD103-SAP (Cat. #IT-50)

Blanco T, Nakagawa H, Musayeva A, Krauthammer M, Singh RB, Narimatsu A, Ge H, Shoushtari SI, Dana R (2024) Acquired immunostimulatory phenotype of migratory CD103+ DCs promotes alloimmunity following corneal transplantation. JCI Insight 9(20):e182469. doi: 10.1172/jci.insight.182469 PMID: 39235864

Objective: To investigate the interaction between antigen-presenting cell subsets, specifically CD11b+ dendritic cells (DC2) and CD103+ dendritic cells (DC1),in the context of transplant immunity.

Summary: The findings highlight the critical role of CD103+ DC1 in modulating host alloimmune responses. In recipients with uninflamed corneal beds, migratory CD103+ DC1 exhibit a tolerogenic phenotype. These cells influence the immunogenic behavior of CD11b+ DC2 primarily through IL-10 production, suppressing alloreactive CD4+ Th1 cells via the PD-L1/PD-1 pathway and promoting Treg-mediated tolerance through αvβ8 integrin–activated TGF-β1. Together, these mechanisms contribute to improved graft survival.

Usage: In vivo depletion of CD103+ DC1: Recipient BALB/c or RAG-/- mice were administered 2.0 mg/kg of Anti-CD103-SAP (IT-50) intraperitoneally, or an equivalent dose of control conjugate (IgG-SAP).

Related Products: Anti-CD103-SAP (Cat. #IT-50), Rat IgG-SAP (Cat. #IT-17)

de Paula FS (2023) Immunomodulatory impact of memory T lymphocyties in periodontitis. Univ Minnesota Thesis.

Objective: This thesis paper sought to determine whether local reactivation of oral tissue resident memory cells (TRM) of a defined antigen specificity could exacerbate ligature-induced periodontal (LIP), a model for periodontal disease in mice.

Summary: Reactivation of oral TRM aggravated alveolar bone loss and amplified gingival and cervical lymph node (cLN) inflammation. Furthermore, oral TRM reactivation enhanced transcriptional changes in pro-inflammatory and periodontitis-related genes. Therapeutic depletion of CD103-expressing oral TRM in advanced of LIP mitigated alveolar bone loss and associated gingiva and cLN inflammation. The study provides evidence that local reactivation of oral TRM can potentiate periodontitis.

Usage: Anti-CD103-SAP (IT-50) was administered in mice via i.p. injection (7 ug in PBS).

Related Products: Anti-CD103-SAP (Cat. #IT-50)

Acovic A, Simovic Markovic B, Gazdic M, Arsenijevic A, Jovicic N, Gajovic N, Jovanovic M, Zdravkovic N, Kanjevac T, Harrell CR, Fellabaum C, Dolicanin Z, Djonov V, Arsenijevic N, Lukic ML, Volarevic V (2018) Indoleamine 2,3-dioxygenase-dependent expansion of T-regulatory cells maintains mucosal healing in ulcerative colitis. Therap Adv Gastroenterol 11:1-22. doi: 10.1177/1756284818793558

Objective: To analyze the significance of the IDO:Treg axis for inducing and maintaining mucosal healing in ulcerative colitis (UC).

Summary: IDO-dependent expansion of endogenous Tregs should be explored as a new approach for induction and maintenance of mucosal healing in patients with UC.

Usage: DSS-treated BALB/c mice were injected with Anti-CD103-SAP (2 mg/kg, intraperitoneally).

Related Products: Anti-CD103-SAP (Cat. #IT-50)

Cao Q, Lu J, Li Q, Wang C, Wang X, Lee V, Wang C, Nguyen H, Zheng G, Zhao Y, Alexander S, Wang Y, Harris D (2016) CD103+ dendritic cells elicit CD8+ t cell responses to accelerate kidney injury in adriamycin nephropathy. J Am Soc Nephrol 27:1344-1360. doi: 10.1681/ASN.2015030229

Summary: Although it is known that dendritic cells (DCs) are involved in chronic kidney disease, it is not well understood how they either resolve or aggravate the condition. CD103+ dendritic cells in particular, are known to maintain tolerance through interaction with regulatory T cells, as well as protect against infection through interactions with CD8+ T cells. In this work the authors depleted CD103+ DCs by administering 1 mg/kg of anti-CD103-SAP (Cat. #IT-50) to the intraperitoneal space of mice subject to adriamycin nephropathy. Rat IgG-SAP (Cat. #IT-17) was used as a control. Elimination of the CD103+ DCs attenuated the kidney injury, indicating that in murine chronic kidney disease CD103+ DCs are pathogenic rather than therapeutic.

Related Products: Anti-CD103-SAP (Cat. #IT-50), Rat IgG-SAP (Cat. #IT-17)

Zhang L, Hadley GA (2010) Application of anti-CD103 immunotoxin for saving islet allograft in context of transplantation. Chin Med J (Engl) 123(24):3644-51.

Summary: This work investigates whether depletion of CD103-positive cells protects transplanted islets from host-immune cell attack. Diabetes was induced in mice, followed by an islet transplant. Anti-CD103-SAP (Cat. #IT-50) was administered via i.p. injection (1.0 mg/kg or 2.0 mg/kg). Rat IgG-SAP (Cat. #IT-17) was used as a control. Diabetic mice treated with anti-CD103-SAP after islet transplantation had an indefinite survival time as compared to untreated mice that survived fewer than 20 days.

Related Products: Anti-CD103-SAP (Cat. #IT-50), Rat IgG-SAP (Cat. #IT-17)

Zhang L, Moffatt-Bruce SD, Gaughan AA, Wang JJ, Rajab A, Hadley GA (2009) An anti-CD103 immunotoxin promotes long-term survival of pancreatic islet allografts. Am J Transplant 9:2012-2023. doi: 10.1111/j.1600-6143.2009.02735.x PMID: 19645708

Objective: To determine whether blockade of the CD103 pathway represents a viable therapeutic strategy for intervention in organ allograft rejection and graft-vs-host disease.

Summary: These data document that depletion of CD103 expressing cells represents a viable strategy for therapeutic intervention in allograft rejection.

Usage: Recipient C57BL/6 mice received 2.0 mg/kg M290-SAP or Rat IgG-SAP on day 3 post-transplantation.

Related Products: Anti-CD103-SAP (Cat. #IT-50), Rat IgG-SAP (Cat. #IT-17)