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

Citation
Kj. Mcelwee et al., Spontaneous alopecia areata-like hair loss in one congenic and seven inbred laboratory mouse strains, J INV D SYM, 4(3), 1999, pp. 202-206
Citations number
26
Categorie Soggetti
Dermatology
Journal title
JOURNAL OF INVESTIGATIVE DERMATOLOGY SYMPOSIUM PROCEEDINGS
ISSN journal
10870024 → ACNP
Volume
4
Issue
3
Year of publication
1999
Pages
202 - 206
Database
ISI
SICI code
1087-0024(199912)4:3<202:SAAHLI>2.0.ZU;2-K
Abstract
Alopecia areata (AA) research has been hampered by the lack of suitable ani mal models for use in experimental procedures. AA-Like hair loss has been o bserved in several species, including dogs, cats, horses, cattle, and nonhu man primates; however, these examples are isolated cases in outbred species of large size, limiting their use in AA research. Inbred rodent strains ar e ideal research models. C3H/HeJ mice can develop spontaneous AA-Like hair loss and have previously been advanced as a suitable experimental model. Th e search for additional mouse strains with AA-like hair loss has continued, Nonscarring, inflammatory, spontaneously reversible hair loss has been obs erved in individual mice from several inbred mouse strains. Aside from C3H/ HeJ mice, an AA-like phenotype has been observed in the substrain C3H/HeJBi r, with an expression frequency of 5%, Up to 10% of individuals in an A/J m ouse colony have been confirmed to develop patchy AA-like hair loss. Isolat ed 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 -H2(h2)/Lil mice, each with a colony frequency of less than 1%. BALB.2R-H2( h2)/Lil mice may also have severe nail defects. AA is regarded as rare in n onhuman 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 analysi s of different AA affected mouse strains may contribute to understanding AA pathogenesis and elucidating susceptibility genes.