Faculty Research 1990 - 1999

Title

Spontaneous alopecia areata-like hair loss in one congenic and seven inbred laboratory mouse strains.

Document Type

Article

Publication Date

1999

Keywords

Animal, Cats, Cattle, Disease-Models-Animal, Dogs, Mice, Mice-Inbred-Strains, Species-Specificity, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-NON-P-H-S, SUPPORT-U-S-GOVT-P-H-S

JAX Source

J Investig Dermatol Symp Proc 1999 Dec; 4(3):202-6.

Grant

CA34196/CA/NCI, AR43801/AR/NIAMS

Abstract

Alopecia areata (AA) research has been hampered by the lack of suitable animal models for use in experimental procedures. AA-like hair loss has been observed in several species, including dogs, cats, horses, cattle, and nonhuman primates; however, these examples are isolated cases in outbred species of large size, limiting their use in AA research. Inbred rodent strains are ideal research models. C3H/HeJ mice can develop spontaneous AA-like hair loss and have previously been advanced as a suitable experimental model. The search for additional mouse strains with AA-like hair loss has continued. Nonscarring, inflammatory, spontaneously reversible hair loss has been observed in individual mice from several inbred mouse strains. Aside from C3H/HeJ mice, an AA-like phenotype has been observed in the substrain C3H/HeJBir, with an expression frequency of 5%. Up to 10% of individuals in an A/J mouse colony have been confirmed to develop patchy AA-like hair loss. Isolated examples of AA have also been identified in C3H/HeN/J mice, C3H/OuJ mice, HRS/J+/hr heterozygous normal mice, CBA/CaHN-Btk(xid)/J mice, and BALB.2R-H2h2/Lil mice, each with a colony frequency of less than 1%. BALB.2R-H2h2/Lil mice may also have severe nail defects. AA is regarded as rare in nonhuman species; however, nonscarring inflammatory based alopecia has been identified in several mouse strains. These examples may represent different subtypes of the heterogeneous AA phenotype. Pathologic and genetic analysis of different AA affected mouse strains may contribute to understanding AA pathogenesis and elucidating susceptibility genes.

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