TY - JOUR
T1 - Tolerance or hypersensitivity to 2,4-dinitro-1-fluorobenzene
T2 - The role of Langerhans cell density within epidermis
AU - Streilein, J. W.
AU - Toews, G. T.
AU - Gilliam, J. N.
AU - Bergstresser, P. R.
N1 - Funding Information:
assistance: Ms. Sabra Sullivan, Ms. Debbie Bate, and Mr. Kevin Stasney. Helpful criticism of the manuscript was provided by Dr. Joan Stein-Streilein. We also appreciate the careful preparation of the manuscript by Ms. Dianna Carey. Dr. Toews was a postdoctoral research fellow sponsored by the Parker B. Francis Foundation.
Funding Information:
Macher and Chase [ 4, 5] proved through a series of elegant, tedious experiments that sensitization following skin painting with hapten required an initial phase during which the hapten reacted directly with a constituent(s) of the skin. Although subsequent processing of this immunogenic signal took place in draining lymph nodes and beyond, the initial, molecular interaction between hapten and a component(s) of skin was essential. It is now known that genes within the major histocompatibility complex (H-2) of the mouse exert profound control over the sensitization process [6]. Vadas et al have shown that the development and successful adoptive transfer of delayed and/ Supported in part by U.S.P.H.S. grants AI-10678, CA-09082, AM-19101 and AM-25563, and by a grant from the Dermatology Foundation. Reprint requests to: J. Wayne Streilein, M.D., Dept. of Cell Biology, U.T.H.S.C.D., 5323 Harry Hines Blvd., Dallas, Texas 75235. Abbreviations: DNFB: 2,4-dinitro-1-fluorobenzene or contact hypersensitivity to DNFB [7], and fowl gamma globulin [8], is restricted by genes of H-2 regions K, I-A, D and I-A, respectively. Shelley and Juhlin [9] have demonstrated that haptenic molecules exposed to the epidermis accumulate preferentially within Langerhans cells.
PY - 1980
Y1 - 1980
N2 - Epidermal Langerhans cells have been implicated in the process by which animals skin painted with highly reactive haptens, such as DNFB, develop contact hypersensitivity. Compared to normal body wall skin, murine tail skin contains relatively few, unevenly distributed Langerhans cells; ultraviolet light exposure depletes the epidermis transiently of normal numbers of morphologically identifiable Langerhans cells. When mice are painted with DNFB on skin naturally or artificially depleted of Langerhans cells, contact hypersensitivity is not induced. More importantly, these animals become specifically unresponsive to the chemical contact, and are unable to mount effective hypersensitivity reactions if presented subsequently with an immunogenic regimen. It is concluded that Langerhans cells provide the skin with an intricate dendritic network just beneath the keratinized layer, the function of which is to receive, process and present cutaneously applied antigens in an immunogenic form. When this barrier network is breached, the host responds to antigenic exposure by becoming profoundly and specifically unresponsive. Implications of this hypothesis for epidermal virus infections and cutaneous malignancy are discussed.
AB - Epidermal Langerhans cells have been implicated in the process by which animals skin painted with highly reactive haptens, such as DNFB, develop contact hypersensitivity. Compared to normal body wall skin, murine tail skin contains relatively few, unevenly distributed Langerhans cells; ultraviolet light exposure depletes the epidermis transiently of normal numbers of morphologically identifiable Langerhans cells. When mice are painted with DNFB on skin naturally or artificially depleted of Langerhans cells, contact hypersensitivity is not induced. More importantly, these animals become specifically unresponsive to the chemical contact, and are unable to mount effective hypersensitivity reactions if presented subsequently with an immunogenic regimen. It is concluded that Langerhans cells provide the skin with an intricate dendritic network just beneath the keratinized layer, the function of which is to receive, process and present cutaneously applied antigens in an immunogenic form. When this barrier network is breached, the host responds to antigenic exposure by becoming profoundly and specifically unresponsive. Implications of this hypothesis for epidermal virus infections and cutaneous malignancy are discussed.
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U2 - 10.1111/1523-1747.ep12543557
DO - 10.1111/1523-1747.ep12543557
M3 - Article
C2 - 7391604
AN - SCOPUS:0018972691
SN - 0022-202X
VL - 74
SP - 319
EP - 322
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 5
ER -