- Email: [email protected]
Immunohistochemical localization of TGF-β in alopecia areata
92
Letters to the Editor
but the meaning of this finding is unclear. The other unprecedented aspect of our case was the PRP-like tinea lesion. It is likely that the intrinsic hyperkeratotic tendency coupled with the immunodepression offers more anaple pabulum for keratophilic organisms, which become able to display unusual pyogenic or keratodermic attitudes, as is our case. Moreover, this case teaches us that a thorough mycological workup (including KOH examination of nails, groin, and various random skin sites) should never be omitted when D o w n ' s patients present with scaling or pustular lesions, in order to avoid misdiagnosis and inappropriate treatment of atypical lesions. Gianfranco Altomare*, Giovanni Luigi Capella, Elena Frigerio, Claudio Fracchiolla
[3] Scherbenske JM, Benson PM, Rotchford JP, James WD. Cutaneous and ocular manifestations of Down syndrome. J Am Acad Dermatol 1990;22:933-938. [4] Rotchford JP, Hyman AB. Extreme hyperkeratotic psoriasis in a mongoloid. Arch Dermatol 1961;83:127-130. [5] Thomas L, Augey F, Chamchikh N, Barrut D, Moulin G. Signes cutan6s de la trisomie 21. Ann Dermatol V6n~r6ol 1994;121:346-350. •[6] Korting GW. Fehlbindungen der Haut und Hautver/inderungen bei Fehlbildungssyndromen. In: Marchionini A Ed. Handbuch der Haut- und Geschlechtskrankheiten(Jadassohn) - Erg/inzungswerk, Vol. 3, Part 1, Berlin: Springer Verlag, 1963;373-493. "[7] Wentscher U, Happle R. Guess what! - Ichthyosiformhyperkeratosis as a characteristic feature of trisomy 21. Eur J Dermatol 1995;5:417-418. [8] Nespoli L, Burgio GR, Ugazio AG, Maccario R. Immunological features of Down's syndrome: a review. J Intellect : DisabRes 1993;37:543-551.
lstituto di Dermatologia, Universit~ degli Studi di Milano, IRCCS Ospedale Maggiore, Via Pace 9, 20122, Milan, Italy
[1] Finzi AF, Altomare GF, BergamaschiniL, Tucci A. Pityriasis rubra pilaris and retinol binding protein. Br J Dermatol 1981 ; 104:253-256. [2] Velthuis PJ, Nijenhuis M. Treatment of onychomycosis with terbinafine in patients with Down's syndrome. Br J Dermatol 1995;133:144-145.
Immunohistochemical alopecia areata
localization of TGF-/3 in
To the Editor: In the July 1996 issue of the Journal of the European Academy of Dermatology and Venereology, Offidani et al. [1] reported on the immunohistochemical localization of transforming growth factor /3 (TGF-/3) in hair follicle epithelium and endothelial cells in alopecia areata patients but not in controls. These authors suggested that TGF-/3 may play a role in matrix degradation and recruitment and stimulation of inflammatory cells and thus may be involved in hair loss. Recently, we studied the expression of TGF-/3 isoforms and their receptors in a mice model with induction of anagen by epilation [2]. We demonstrated that TGF-/3's and the receptor type I (T/3R-I) are expressed in hair follicle epithelium and latent TGF-/3 protein in the sebaceous glands. In early anagen the inner hair root sheath was stained with TGF/31 antibodies, whereas the outer hair root sheath was positive for T/3R-I during the anagen catagen switch.
• Correspondingauthor. Tel.: +39 2 55035123/5463628; fax: +39 2 55195997. PIt: S0926-9959(97)00089-5
Furthermore, we found a significant expression of T/3R-I and -II in sebocytes, which seems to argue for a bidirectional growth control of sebaceous glands and hair follicle epithelium. Our findings are in favor of the following hypothesis: TGF-/31 releases by inner hair root epithelium may regulate the outer sheath growth. TGF-/3 may function as growth inhibitor at the anagen catagen switch [2]. In these animals no inflammatory infiltrate is present. If TGF-/3 is involved in the recruitment of leukocytes and other inflammatory cells as suggested by Offidani et al. [1] it must be released by endothelial cells. The data would also support that TGF-/3 involvement in the extracellular matrix production is, at least in mice, not restricted to pathological conditions but is found during the normal hair cycle as well. Since there is a marked increase in telogen follicle counts in alopecia areata, the overexpression of TGF/3 might be involved in the faster anagen-catagentelogen switch. We would like to thank these author for indicating TGF-/3 as a possible factor in hair growth control in humans but our data in the animal
Letters to the Editor
model would suggest a broader role of TGF-/3 in hair physiology than that suggested by Offidani et al, [1]. U. Wollina*'*, D. Lange a, K. Funa b, R. Paus c
aDepartment of Dermatology, Friedrich-Schiller, University of ,lena, 07740 Jena, Germany bLudwig Institute for Cancer Research, Biomedical Center. Uppsala, Sweden CDepartment of Dermatology, Alexander-yon-Humboldt-University (CharitE), Berlin, Germany
[1] Offidani A, Lucarini G, Cellini A, Simonetti O, Nicoloni M, Biagini G, Castaldini C. Immunohistochemical localization of TGF-B in the skin of patients with alopecia areata. J Eur Acad Dermatol Venereol 1996;7:75-77. 12] Wollina U, Lange D, Funa K, Pans R. Expression of transforming growth factor ~ isoforms and their receptors during hair growth phases in mice. Histol Histopathol 1996;11:431436.
° Corresponding author.
93
The authors reply To the Editor: Alopecia areata (AA) is an immunologic mediated disease in which inflammatory cytokines probably play a major role. We would like to thank Dr. Wollina and colleagues for pointing out the probable role of TGF-fl in the growth of hair follicle, but we focused our study on the inflammatory aspect of AA pathogenesis and we do not think that the mice model proposed by Wollina and colleagues would be applicable to the AA study. Nevertheless, we agree with Dr. Wollina in the statement that TGF-/3 could have a broader role in hair root physiology and development. A. Oflidani a'*, G. Lucarini b, A. Cellini a, O. Simonetfi a, M. Nicolini*, G. Biagini b, C. Castaldini c
°Institute of Dermatology, University of Ancona, Ancona, Italy blnstitute of Normal Human Morphology, University of Ancona, Ancona, Italy Clnstitute of Histology, University of Bologna, Bologna. Italy
PII: S0926-9959(97)00090-1
"Corresponding author. PII: S0926-9959(97)00091-3
Letters to the Editor
but the meaning of this finding is unclear. The other unprecedented aspect of our case was the PRP-like tinea lesion. It is likely that the intrinsic hyperkeratotic tendency coupled with the immunodepression offers more anaple pabulum for keratophilic organisms, which become able to display unusual pyogenic or keratodermic attitudes, as is our case. Moreover, this case teaches us that a thorough mycological workup (including KOH examination of nails, groin, and various random skin sites) should never be omitted when D o w n ' s patients present with scaling or pustular lesions, in order to avoid misdiagnosis and inappropriate treatment of atypical lesions. Gianfranco Altomare*, Giovanni Luigi Capella, Elena Frigerio, Claudio Fracchiolla
[3] Scherbenske JM, Benson PM, Rotchford JP, James WD. Cutaneous and ocular manifestations of Down syndrome. J Am Acad Dermatol 1990;22:933-938. [4] Rotchford JP, Hyman AB. Extreme hyperkeratotic psoriasis in a mongoloid. Arch Dermatol 1961;83:127-130. [5] Thomas L, Augey F, Chamchikh N, Barrut D, Moulin G. Signes cutan6s de la trisomie 21. Ann Dermatol V6n~r6ol 1994;121:346-350. •[6] Korting GW. Fehlbindungen der Haut und Hautver/inderungen bei Fehlbildungssyndromen. In: Marchionini A Ed. Handbuch der Haut- und Geschlechtskrankheiten(Jadassohn) - Erg/inzungswerk, Vol. 3, Part 1, Berlin: Springer Verlag, 1963;373-493. "[7] Wentscher U, Happle R. Guess what! - Ichthyosiformhyperkeratosis as a characteristic feature of trisomy 21. Eur J Dermatol 1995;5:417-418. [8] Nespoli L, Burgio GR, Ugazio AG, Maccario R. Immunological features of Down's syndrome: a review. J Intellect : DisabRes 1993;37:543-551.
lstituto di Dermatologia, Universit~ degli Studi di Milano, IRCCS Ospedale Maggiore, Via Pace 9, 20122, Milan, Italy
[1] Finzi AF, Altomare GF, BergamaschiniL, Tucci A. Pityriasis rubra pilaris and retinol binding protein. Br J Dermatol 1981 ; 104:253-256. [2] Velthuis PJ, Nijenhuis M. Treatment of onychomycosis with terbinafine in patients with Down's syndrome. Br J Dermatol 1995;133:144-145.
Immunohistochemical alopecia areata
localization of TGF-/3 in
To the Editor: In the July 1996 issue of the Journal of the European Academy of Dermatology and Venereology, Offidani et al. [1] reported on the immunohistochemical localization of transforming growth factor /3 (TGF-/3) in hair follicle epithelium and endothelial cells in alopecia areata patients but not in controls. These authors suggested that TGF-/3 may play a role in matrix degradation and recruitment and stimulation of inflammatory cells and thus may be involved in hair loss. Recently, we studied the expression of TGF-/3 isoforms and their receptors in a mice model with induction of anagen by epilation [2]. We demonstrated that TGF-/3's and the receptor type I (T/3R-I) are expressed in hair follicle epithelium and latent TGF-/3 protein in the sebaceous glands. In early anagen the inner hair root sheath was stained with TGF/31 antibodies, whereas the outer hair root sheath was positive for T/3R-I during the anagen catagen switch.
• Correspondingauthor. Tel.: +39 2 55035123/5463628; fax: +39 2 55195997. PIt: S0926-9959(97)00089-5
Furthermore, we found a significant expression of T/3R-I and -II in sebocytes, which seems to argue for a bidirectional growth control of sebaceous glands and hair follicle epithelium. Our findings are in favor of the following hypothesis: TGF-/31 releases by inner hair root epithelium may regulate the outer sheath growth. TGF-/3 may function as growth inhibitor at the anagen catagen switch [2]. In these animals no inflammatory infiltrate is present. If TGF-/3 is involved in the recruitment of leukocytes and other inflammatory cells as suggested by Offidani et al. [1] it must be released by endothelial cells. The data would also support that TGF-/3 involvement in the extracellular matrix production is, at least in mice, not restricted to pathological conditions but is found during the normal hair cycle as well. Since there is a marked increase in telogen follicle counts in alopecia areata, the overexpression of TGF/3 might be involved in the faster anagen-catagentelogen switch. We would like to thank these author for indicating TGF-/3 as a possible factor in hair growth control in humans but our data in the animal
Letters to the Editor
model would suggest a broader role of TGF-/3 in hair physiology than that suggested by Offidani et al, [1]. U. Wollina*'*, D. Lange a, K. Funa b, R. Paus c
aDepartment of Dermatology, Friedrich-Schiller, University of ,lena, 07740 Jena, Germany bLudwig Institute for Cancer Research, Biomedical Center. Uppsala, Sweden CDepartment of Dermatology, Alexander-yon-Humboldt-University (CharitE), Berlin, Germany
[1] Offidani A, Lucarini G, Cellini A, Simonetti O, Nicoloni M, Biagini G, Castaldini C. Immunohistochemical localization of TGF-B in the skin of patients with alopecia areata. J Eur Acad Dermatol Venereol 1996;7:75-77. 12] Wollina U, Lange D, Funa K, Pans R. Expression of transforming growth factor ~ isoforms and their receptors during hair growth phases in mice. Histol Histopathol 1996;11:431436.
° Corresponding author.
93
The authors reply To the Editor: Alopecia areata (AA) is an immunologic mediated disease in which inflammatory cytokines probably play a major role. We would like to thank Dr. Wollina and colleagues for pointing out the probable role of TGF-fl in the growth of hair follicle, but we focused our study on the inflammatory aspect of AA pathogenesis and we do not think that the mice model proposed by Wollina and colleagues would be applicable to the AA study. Nevertheless, we agree with Dr. Wollina in the statement that TGF-/3 could have a broader role in hair root physiology and development. A. Oflidani a'*, G. Lucarini b, A. Cellini a, O. Simonetfi a, M. Nicolini*, G. Biagini b, C. Castaldini c
°Institute of Dermatology, University of Ancona, Ancona, Italy blnstitute of Normal Human Morphology, University of Ancona, Ancona, Italy Clnstitute of Histology, University of Bologna, Bologna. Italy
PII: S0926-9959(97)00090-1
"Corresponding author. PII: S0926-9959(97)00091-3