Comparative Study on Picryl Chloride (PCL)-Induced Contact Dermatitis in Female IQI/Jic and BALB/c Mice.

Jung, Ji‐Youn; Saegusa, Junzo; Nakayama, Hiroyuki; Doi, Kunio

doi:10.1538/expanim.53.89

Cited by 11 publications

(4 citation statements)

References 20 publications

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“…In addition, lymphocytic infiltration can occur in multiple exocrine and non-exocrine organs, such as pancreas, kidneys, and lungs [104]. As such, this strain has been used for the study of other diseases, such as dermatitis [105], colitis [106] and adrenal cell hyperplasia [107]. Of note, ANA were detected but neither anti-SSA/Ro nor anti-SSB/La autoantibodies were detected from their sera [103].…”

Section: Mouse Modelsmentioning

confidence: 99%

Mouse Models of Primary Sjogren’s Syndrome

Park¹,

Gauna²,

Cha

2015

CPD

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Sjögren’s syndrome (SjS) is a chronic autoimmune disorder characterized by immune cell infiltration and progressive injury to the salivary and lacrimal glands. As a consequence, patients with SjS develop xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes). SjS is the third most common rheumatic autoimmune disorder, affecting 4 million Americans with over 90% of patients being female. Current diagnostic criteria for SjS frequently utilize histological examinations of minor salivary glands for immune cell foci, serology for autoantibodies, and dry eye evaluation by corneal or conjunctival staining. SjS can be classified as primary or secondary SjS, depending on whether it occurs alone or in association with other systemic rheumatic conditions, respectively. Clinical manifestations typically become apparent when the disease is relatively advanced in SjS patients, which poses a challenge for early diagnosis and treatment of SjS. Therefore, SjS mouse models, because of their close resemblance to the human SjS, have been extremely valuable to identify early disease markers and to investigate underlying biological and immunological dysregulations. However, it is important to bear in mind that no single mouse model has duplicated all aspects of SjS pathogenesis and clinical features, mainly due to the multifactorial etiology of SjS that includes numerous susceptibility genes and environmental factors. As such, various mouse models have been developed in the field to try to recapitulate SjS. In this review, we focus on recent mouse models of primary SjS and describe them under three categories of spontaneous, genetically engineered, and experimentally induced development of SjS-like disease. In addition, we discuss future perspectives of SjS mouse models highlighting pros and cons of utilizing mouse models and demands for improved models.

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Section: Mouse Modelsmentioning

confidence: 99%

Mouse Models of Primary Sjogren’s Syndrome

Park¹,

Gauna²,

Cha

2015

CPD

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“…In toluidine blue-stained sections, the number of mast cells was evaluated with an area of 30 to 40%, in toluidine-stained slides using microscopy and ImageJ software. 39 …”

Section: Methodsmentioning

confidence: 99%

Chitosan hydrogel for topical delivery of ebastine loaded solid lipid nanoparticles for alleviation of allergic contact dermatitis

et al. 2021

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“…Several investigators have reported mouse strain-associated differences in susceptibility to hapten-induced CHS [8,9,10]. The differences among mouse strains in terms of severity of skin inflammation are often related to the degree of expansion of different helper T cell types (Th1 or Th2) that mediate the CHS response.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-5 Plays a Key Role in Mouse Strain- Dependent Susceptibility to Contact Hypersensitivity through Its Effects on Initiator B Cells

Itakura

Ikutani

Takatsu

et al. 2013

Int Arch Allergy Immunol

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Background: Elicitation of contact hypersensitivity requires antigen-specific immunoglobulin M (IgM) antibodies that trigger recruitment of effector T cells to the local tissue. These antigen-specific IgM antibodies are produced by B-1-like ‘initiator B cells'. In this study, we compared susceptibility to hapten-induced contact hypersensitivity between BALB/c and C57BL/6 mice. Methods: BALB/c and C57BL/6 mice were sensitized by painting oxazolone onto the skin and were challenged on the ears with the same hapten on day 4. Ear thickness and serum hapten-specific IgM levels were measured at 24 h post-challenge. Peritoneal cells were harvested and the numbers of B cell subpopulations were counted. Interleukin (IL)-5 was intraperitoneally injected into BALB/c and C57BL/6 mice, and the change in numbers of B cell subpopulations and serum IgM levels was monitored. Results: Oxazolone induced stronger ear swelling and specific IgM responses in BALB/c mice than in C57BL/6 mice. BALB/c mice had higher numbers of peritoneal B-1 cells than C57BL/6 mice at steady state. IL-5 injection increased the number of peritoneal B-1 cells and serum IgM levels more significantly in BALB/ mice than in C57BL/6 mice. Conclusions: BALB/c mice exhibit higher susceptibility to hapten-induced contact hypersensitivity than C57BL/6 mice, most likely because they have a higher number of B-1 cells, leading to massive production of hapten-specific IgM antibodies upon contact sensitization. The differences in the number of B-1 cells and IgM responses between the two strains of mice may be attributed to the difference in responsiveness of B-1 cells to IL-5.

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Comparative Study on Picryl Chloride (PCL)-Induced Contact Dermatitis in Female IQI/Jic and BALB/c Mice.

Cited by 11 publications

References 20 publications

Mouse Models of Primary Sjogren’s Syndrome

Mouse Models of Primary Sjogren’s Syndrome

Chitosan hydrogel for topical delivery of ebastine loaded solid lipid nanoparticles for alleviation of allergic contact dermatitis

Interleukin-5 Plays a Key Role in Mouse Strain- Dependent Susceptibility to Contact Hypersensitivity through Its Effects on Initiator B Cells

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