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Autoimmune Pancreatitis (AIP)

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Autoimmune pancreatitis (AIP) refers to a particular subtype or type of chronic pancreatitis that stems from an autoimmune response and manifests through inflammation and fibrosis of the pancreas. At Protheragen, we focus on furthering drug development efforts for rare gastrointestinal disorders, with a special emphasis on AIP. Our goal is to comprehensively develop research that addresses the complex nature of this condition and provide integrated therapy development services.

Overview of Autoimmune Pancreatitis (AIP)

Autoimmune pancreatitis (AIP) is defined as a type of pancreatitis that is characterized by obstructive jaundice with or without pancreatic masses, lymphoplasmacytic infiltrate fibrosis, and a marked response to steroids. The yearly incidence was 3.1 per population of 100,000 people. AIP can be divided into type 1 (AIP-1), also known as lymphoplasmacytic sclerosing pancreatitis (LPSP), and type 2 (AIP-2), also called idiopathic ductal centric pancreatitis (IDCP). There has been recently described AIP: Type 3 AIP (AIP-3) is a mostly asymptomatic or rarely pauci-symptomatic form of pancreatic injury that exclusively affects individuals with advanced malignancies.

Fig.1 IgG4-RD phenotypes. (Nista, E. C., et al., 2022)

Pathogenesis of Autoimmune Pancreatitis (AIP)

All AIPs have differing approaches both on how they are caused by illness and how they progress. AIP-1, AIP-2, and AIP-3 are distinct from each other at the level of their epidemiology, pathogenesis, histologic pattern, and natural history.

The manifestation of IgG4-RD type AIP-1 is pancreatic. After the action of TLRs on MHC-II, there is activation of T helper and Treg CD4⁺ lymphocytes. Furthermore, T follicular helper (Tfh) cells and SLAMF7 interact, facilitating the release of IgG4.

About AIP-2 pathogenesis, a special role is reserved for the Th-17 subpopulation of CD4+ effector T cells, which infiltrates the periductal pancreatic tissues and produces a variety of inflammatory cytokines including IL-17, IL-21, IL-22, and IL-23.

The etiology of AIP-3 is more associated with the use of checkpoint inhibitors which gives rise to non-specific inflammatory immune responses that are T-cell mediated, particularly with CD8⁺ T cells which causes an increase in CD8⁺/CD4⁺ T lymphocyte ratio.

Fig.2 Etiopathology of various AIP types. (Gallo, C., et al., 2024)

Therapeutics Development for Autoimmune Pancreatitis (AIP)

Drug Names	Mechanism of Action	Targets	NCT Number	Research Phase
Rituximab	Lessening the rate of new plasma cell production or the disruption of another function that B cells have in the immune system.	CD20	NCT01584388	Phase II
Corticosteroids	Obstructing the entry of neutrophils and monocytes to the area of inflammation.	GR	NCT02797665	N/A
Lenalidomide	Exerts immunomodulating effects through changes in cytokine production, T cell co-stimulation, and NK cell-mediated cytotoxicity enhancement.	CK1α	NCT02705638	Phase I
Leflunomide	A new generation immunomodulating drug that has potent NF-κB activation blocking properties.	DHODH	NCT02703194	Phase IV

Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.

Our Services

With our bespoke services in diagnostics, therapeutic, and disease model development, we specialists fulfill the needs of researchers and scientists, while also making our services available for projects across the board. In addition to offering preclinical services for AIP drug discovery and development, we also offer a complete set of services that include pharmacology, pharmacokinetics, and drug safety evaluation.

Therapeutic Development Services

Animal Model Development Services

Animal models of AIP are essential for understanding the potential mechanisms underlying the disease and its corresponding therapies. Our company offers all-inclusive animal model development services to provide value in understanding the physiopathology of AIP while enhancing novel therapeutic approaches.

Genetically Engineering Model

The genetically engineered Tg(Ela1-Lta,b) model represents a genetic model where AIP develops spontaneously.

CD4⁺ T Cell Transfer Model

The CD4⁺ T Cell Transfer model utilizes the adoptive transfer of amylase-specific CD4⁺ T cells into syngeneic recipient animals to induce AIP.

Polyinosinic-polycytidylic acid (poly (I: C))-induced Model

The model involves the use of autoimmune-prone MRL/Mp or IL-10^-/- mice, which are treated with repeated injections of poly (I: C).

Escherichia coli-induced Model

Animals are subjected to intraperitoneal administration of Escherichia coli, leading to persistent exposure that induces AIP.

Protheragen's dedication to enhancing novel drug development for this condition positions us as a leader in the field. Contact us today to find out how our expert services can enhance your drug development endeavors for AIP and other rare gastrointestinal diseases.

References

Nista, Enrico Celestino et al. "Autoimmune Pancreatitis: From Pathogenesis to Treatment." International journal of molecular sciences 23.20 (2022): 12667.
Gallo, Camilla et al. "Autoimmune pancreatitis: Cornerstones and future perspectives." World journal of gastroenterology 30.8 (2024): 817-832.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.