PubMed Health⌕ Search

Biomedical subjects

S R Lessin

Publications and source records attributed to S R Lessin.

At least 37 records · Page 2Linked to original sources
PubMed1997

The pathogenesis of large cell transformation in cutaneous T-cell lymphoma is not associated with t(2;5)(p23;q35) chromosomal translocation.

In 20%-50% of the advanced cutaneous T-cell lymphomas (CTCL), malignant T cells undergo large cell transformation (LCT). The malignant T cells of LCT in CTCL can share morphologic and immunophenotypic similarities with CD30 (Ki-1)-positive anaplastic large cell lymphoma (ALCL), suggesting a common mechanism of pathogenesis. The t(2;5) (p23;q35) translocation, resulting in the fusion of the nucleophosmin (NPM) gene and the anaplastic lymphoma kinase (ALK) gene, is associated with primary CD30+ ALCL. To determine whether acquisition of this chromosomal translocation is involved in the pathogenesis of LCT in CTCL, we examined 12 tumor samples from 9 CTCL patients, including 8 with LCT-CTCL and one with concurrent CTCL and Hodgkin's disease, for the presence of the t(2;5) translocation. Numerous CD30+ large cells were present in 4 LCT-CTCL consistent with secondary CD30+ ALCL; CD30 was expressed by <10% of the large cells in another case and was negative in the other 3 lymphomas. Using primers spanning the NPM/ALK fusion junction, PCR amplification following reverse transcription (RT) of mRNA failed to show the products of NPM/ALK fusion in all samples tested. Thus, the t(2;5) (p23;q35) translocation does not appear to be involved in the molecular pathogenesis of LCT in CTCL, including CD30+ cases.

Cell Transformation, Neoplastic↗
PubMed1997

Folliculotropic mycosis fungoides with large-cell transformation presenting as dissecting cellulitis of the scalp.

Follicular mycosis fungoides (MF) is a rare variant of cutaneous T-cell lymphoma (CTCL) in which malignant lymphocytes preferentially infiltrate hair follicles. This report describes a patient with follicular mycosis fungoides presenting in a manner similar to dissecting cellulitis of the scalp with nonhealing, draining nodular lesions. Follicular mucinosis associated with folliculotropic mycosis fungoides resulted in follicular disruption and deep dissecting cellulitis. Large-cell transformation of CTCL was present in the initial diagnostic scalp and axillary lymph node specimens. The patient died from progressive CTCL 9 months following initial diagnosis despite electron beam radiation, topical mechlorethamine, interferon-alpha, and systemic chemotherapy. This case indicates that large-cell transformation of folliculotropic mycosis fungoides is an aggressive form of CTCL, and that folliculotropic mycosis fungoides can give rise to lesions which resemble dissecting cellulitis of the scalp. Upregulation of intercellular adhesion molecule-1 (ICAM-1) on follicular epithelium adjacent to lymphocyte function-associated antigen-1 (LFA-1)-positive folliculotropic lymphoma cells in this report provides insight into lymphocyte homing mechanisms in folliculotropic MF.

Adult↗
PubMed1997

Pathogenesis of cutaneous T-cell lymphoma: implications for the use of recombinant cytokines and photopheresis.

Cutaneous T-cell lymphoma (CTCL) is a clonally derived, skin invasive malignancy of CD4+ cells with the phenotype of mature helper T cells. We previously demonstrated that the leukaemic form of CTCL (Sézary), is characterized by prominent immunological defects including depressed cell-mediated immunity. We also demonstrated increased production of T-helper type 2 (Th2) cytokines (IL-4, IL-5) and deficient Th1 cytokines (IL-2 and IFN-gamma) by their peripheral blood mononuclear cells (PBMC) and detected IL-4 and IL-5 mRNA within lesional skin of patients with all stages of CTCL. A marked defect in IL-12 production has also been noted, which may also play a role in depressed cell-mediated immunity. These results suggested that the malignant CD4+ cells were Th2 cells. Thus, the immune aberrations have been attributed to the cytokine abnormalities triggered by the malignant T-cell population. Because CTCL responds to biological response modification, we focused on strategies for reversing the cytokine and immune defects by in vitro testing of novel biological response modifiers. Our results indicate that IFN-alpha potently suppresses the abnormal IL-4 and IL-5 production, that IL-12 can correct the deficient IFN-gamma production and cell-mediated cytotoxicity, and that retinoids can enhance IFN-gamma and IL-12 production. We also studied the in vitro growth characteristics of the malignant CD4+ cells and determined that IL-12 and IFN-alpha significantly suppress growth of these cells. These studies led to a phase I trial of IL-12 to treat CTCL. Also, we have determined that photopheresis produces a high clinical response rate among Sézary syndrome patients. This therapy not only augments functions of monocytes but also induces the malignant T cells to undergo a high rate of apoptosis. We discuss how these therapies might be employed in concert to produce the optimum desired anti-tumour effect.

Animals↗
PubMed1996

The potential therapeutic role of interleukin-12 in cutaneous T-cell lymphoma.

Cutaneous T-cell lymphoma (CTCL) is a lymphoproliferative disorder characterized by skin invasion of clonally derived malignant CD4+ lymphocytes that phenotypically resemble mature T-helper (Th) cells. Sezary syndrome (SzS) represents an advanced form of CTCL associated with generalized erythroderma and involvement of the peripheral blood by the malignant cell population. We have previously demonstrated aberrant cytokine production by peripheral blood mononuclear cells (PBMCs) in SzS characterized by increased IL-4 and deficient IL-2 and IFN-gamma production, as well as increased expression of mRNA for IL-4 and IL-5 within active skin lesions, indicating that the clonal T-cell population is likely derived from the T-helper type 2 (Th2) subset of helper T lymphocytes. Furthermore, a variety of immune abnormalities have been observed in association with SzS that have been attributed to the cytokine abnormalities. Because IL-12 is a potent inducer of IFN-gamma production and causes the activation of cytotoxic lymphocytes, we assessed the production of IL-12 by PBMCs from SzS patients, and whether IL-12 could alter the unfavorable cytokine balance typical of SzS and, thus, possibly lead to correction of immune defects. In this review, we present our data, which indicate that patients with SzS exhibit marked defects in monocyte production of IL-12 p70. Moreover, in vitro culture of PBMC from SzS patients with recombinant IL-12 leads to reconstitution of normal IFN-gamma production and markedly enhances cell-mediated cytotoxicity.

Cells, Cultured↗
PubMed1996

IL-12 synthesis by human Langerhans cells.

IL-12 is a 70-kDa heterodimeric cytokine composed of a p35 chain and p40 chain. This cytokine exerts a powerful positive regulatory influence on the development of Th1 helper T-cell immune responses and is a potent inducer of IFN-gamma production and cytotoxic T cell differentiation and function. Because epidermal Langerhans cells (LC) are important members of the dendritic APC lineage family critical for initiating cell mediated immune responses, we examined LC for their ability to produce IL-12. Epidermal cell (EC) suspensions obtained from volunteers were enriched for, or depleted of, Langerhans cells (CD1a+ EC). Enriched populations contained > 90% CD1a+ cells, whereas depleted populations contained < 1% CD1a+ cells. As assessed by reverse transcription-PCR amplification, IL-12 p40 mRNA was constitutively expressed in LC RNA extracted immediately following keratome harvest, and increased spontaneously after overnight incubation. Radioimmunoassay (RIA) of IL-12 p40 protein on supernatants revealed IL-12 release by CD1a-enriched fractions of epidermal cells. Ab specific for p40 clearly demonstrated IL-12 in epidermal LC by flow cytometry. A bioassay for the functional IL-12 heterodimer (p70) indicated that LC could produce IL-12 biologic activity, which was neutralized by anti-IL-12 Ab. These results indicate that epidermal LC, in particular cultured LC maturing into dendritic cells, express IL-12 p40 mRNA, as well as p40 and functional p70 protein, and suggest that this is one mechanism behind the high potency of dendritic APCs, such as LC, to initiate Th1 type immune responses under appropriate conditions.

Adult↗
PubMed1996

Treatment of cutaneous T-cell lymphoma with extracorporeal photopheresis monotherapy and in combination with recombinant interferon alfa: a 10-year experience at a single institution.

BACKGROUND: Extracorporeal photopheresis is a pheresis-based therapy that permits the direct targeting of psoralen-mediated photochemotherapy to circulating pathogenic T cells. Although photopheresis is currently used to treat cutaneous T-cell lymphoma (CTCL), limited data are available regarding overall response rates and durability of responses among patients with advanced disease. Furthermore, little is known about the effectiveness and tolerability of combined regimens employing other biologic response modifiers including interferon alfa. OBJECTIVE: Our purpose was to determine the efficacy of photopheresis among 41 patients with the clinical and laboratory diagnosis of CTCL; the majority of patients had stage III or IV disease with the presence of circulating malignant T cells. METHODS: A retrospective chart review during a 10-year period at a single university hospital was performed for all patients receiving either photopheresis monotherapy on two consecutive days every 4 weeks (one cycle) and for an additional 12 patients who also received interferon alfa 1.5 to 5 million U subcutaneously three to five times weekly. RESULTS: Thirty-one of 41 patients (76%) were treated for six or more cycles. The remaining 10 were treated with less than six cycles because of rapidly progressing disease (n = 6), death unrelated to CTCL (n = 2), or withdrawal from treatment (n = 1); one of the 10 patients had only received five cycles of treatment but is still receiving therapy. Twenty-eight of the 31 patients treated for six or more cycles received photopheresis alone. Among the 28, seven patients (25%) had a complete remission, 13 (46%) had a partial remission defined as more than 50% clearing of skin disease, and eight (29%) did not respond to treatment. The presence of Sézary cells in the peripheral blood was associated with a favorable response. Median time to treatment failure was 18 months, whereas median survival from initiation of therapy was 77 months and from the time of diagnosis exceeded 100 months. Nine of these 28 patients went on to receive combination therapy with interferon alfa and, in some cases, other agents. Among these nine patients, five had an enhanced clinical response to the combination therapy compared with treatment with photopheresis monotherapy. The combined regimen was well tolerated. CONCLUSION: These results indicate that patients with advanced CTCL can achieve a high response rate for an extended period with photopheresis and that interferon alfa combined with photopheresis is a well-tolerated regimen that appears to produce higher response rates than photopheresis alone.

Adult↗
PubMed1996

Failure to detect human T-lymphotropic virus type-I proviral DNA in cell lines and tissues from patients with cutaneous T-cell lymphoma.

Previous molecular studies investigating the presence of HTLV-I proviral DNA in cell lines and tissue samples of patients with cutaneous T-cell lymphoma (CTCL) have reported a detection rate ranging from 0-92%. Despite the lack of epidemiologic data linking HTLV-I infection with CTCL, the molecular data still invite speculation regarding the precise role of HTLV-I in the pathogenesis of CTCL. To determine the detection rate of HTLV-I proviral DNA among CTCL patients referred to our medical center, we analyzed Epstein-Barr virus-transformed cell lines established from peripheral blood of seven CTCL patients and 43 tissue samples from 22 patients with different stages of disease. Genomic DNA was polymerase chain reaction-amplified with primers within the HTLV-I tax gene region. Amplification products were probed with nested oligonucleotide probes by Southern blot analysis. No HTLV-I proviral sequences were detected in the samples (0/50). Using HTLV-I/II pol primers, no HTLV-I pol gene sequences were detected. In tissues from one patient, HTLV-II pol and tax gene sequences were detected; however, HTLV-II proviral integration was not detected by Southern blot analysis of the genomic DNA. Our data suggest: (i) HTLV-I does not appear to be a primary etiologic agent in CTCL; and (ii) HTLV-II pol and tax gene sequences can be detected in a minority of CTCL patients, but this does not necessarily imply an etiologic role.

Base Sequence↗
PubMed1996

Correlation between clonotypic T-cell receptor beta chain variable region (TCR-V beta) gene expression and aberrant T-cell antigen expression in cutaneous T-cell lymphoma.

Immunohistochemical studies can augment the clinicopathologic diagnosis of cutaneous T-cell lymphoma (CTCL). Our goal was to determine whether a panel of 11 T-cell receptor (TCR) beta chain variable region (V beta) monoclonal antibodies (moAbs) could consistently identify clonal T-cell populations within CTCL skin infiltrates, and whether these cell exhibited aberrant T-cell antigen expression. Biopsies from 24 CTCL and 3 parapsoriasis patients were analyzed. Of the 27 patients, 4 (15%) demonstrated T-cell clonality by restricted TCR-V beta moAb staining. The V beta + restricted cells expressed aberrant antigen profiles. Overall, aberrant antigen profiles were detected in 18/24 (75%) CTCL. Patients. V beta 18 moAb crossreacted with a 85 kD protein produced by basal and suprabasal keratinocytes. We conclude: 1) Restricted TCR-V beta expression correlated with aberrant T-cell antigen profiles: 2) In the absence of a complete panel of TCR-V beta moAbs, localization of aberrant T-cell antigen expression can be useful in identifying malignant T-cells within CTCL skin infiltrates; 3) The detection sensitivity and specificity of the currently available TCR-V beta moAbs may limit their utility to consistently detect clonal T-cell populations in CTCL skin biopsies; 4) A 85 kD protein present on basal and suprabasal keratinocytes is recognized by V beta 18 moAb and may be related to immune function(s) of the epidermis.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1996

The role of alpha E beta 7 integrin (CD103) and E-cadherin in epidermotropism in cutaneous T-cell lymphoma.

Adhesion molecules such as integrins and cadherins are thought to play a critical role in T-cell migration and localization within the epidermis (epidermotropism). The purpose of this study was to correlate T-cell expression of the integrin CD103 and E-cadherin in cutaneous T-cell lymphoma (CTCL). Serial sections of skin biopsies from 22 patients with CTCL and 13 with benign reactive dermatitis were stained with antibodies to CD4, CD103, and E-cadherin by the avidin-biotin peroxidase technique. CD103 was expressed on single epidermotropic CD4+ T-cells in 9/9 early stage (patch/plaque) CTCL and 6/10 reactive dermatitis biopsies. Less than 30% of dermal T-cells expressed CD103. All 4/4 late stage (tumor) CTCL were CD103-. Epidermal aggregates of CD4+ T-cells (Pautrier's microabscesses) were CD103-. E-cadherin was expressed on epidermal keratinocytes and follicular and sweat gland epithelia but not on T-cells. We conclude that CD103 expression on cutaneous T-cells parallels the degree of epidermotropism exhibited in both neoplastic and inflammatory disorders of the skin. E-cadherin is not expressed on T-cells infiltrating the skin. Further investigation is necessary to further elucidate the interaction between CD103 and E-cadherin in facilitating trafficking of T-cells into the epidermis.

Antigens, CD↗
PubMed1996

Increased serum concentration of the soluble interleukin-2 receptor in cutaneous T-cell lymphoma. Clinical and prognostic implications.

BACKGROUND AND DESIGN: The serum concentration of soluble alpha-chain receptor for interleukin-2 (sIL-2R) was determined in 101 patients with cutaneous T-cell lymphoma (CTCL). RESULTS: The serum concentration of sIL-2R correlates positively with CTCL tumor burden as determined by several clinical parameters (ie, clinical subtype of disease, extent of skin involvement, T rating, and stage), by serum lactate dehydrogenase concentration, and by Sézary cell counts in erythrodermic disease. The median value of sIL-2R in erythrodermic CTCL was more than threefold higher than that of classic mycosis fungoides (MF). The proportion of patients with elevated sIL-2R concentration (> 1000 U/mL) also increased in CTCL in a similar fashion according to the clinical type of disease (MF patch phase, 15%; MF plaque phase, 33%; MF tumor phase, 47%; and erythrodermic variants, 90%). However, no correlation was found between sIL-2R serum concentration and expression of membrane-bound IL-2R alpha chain (CD25) on lymphoid cells in skin lesions and peripheral blood. Significantly, multivariate analysis of various prognostic factors demonstrated that in erythrodermic CTCL, sIL-2R serum concentration correlated best with survival and was a better predictor of prognosis than stage, Sézary cell counts, or lactate dehydrogenase values. CONCLUSIONS: These findings document the usefulness of the measurement of the sIL-2R serum concentration to determine tumor burden and prognosis in patients with CTCL.

Adult↗
PubMed1995

The clonal nature of circulating Sezary cells.

To determine if circulating Sezary cells can be classified as reactive or neoplastic based on the ability to detect the presence or absence of clonal T-cell receptor beta chain (TCR-beta) gene rearrangements by Southern blot analysis, we evaluated the peripheral blood of 25 patients: 11 patients with Sezary syndrome (SS), 11 with benign inflammatory dermatoses (BID), and three normal controls. Three of 11 patients with SS, with Sezary counts ranging from 14% to 52%, did not demonstrate any clonal TCR-beta gene rearrangements in the peripheral blood, despite a TCR-beta rearrangement by Southern blot analysis in the skin. Ten of 11 BID patients and all normal controls showed no evidence of a TCR-beta gene rearrangement in the peripheral blood. However, one patient with psoriasis demonstrated a TCR-beta gene rearrangement in the peripheral blood. The TCR-beta gene rearrangement detected in this patient, confirmed with polymerase chain reaction (PCR) amplification of the TCR-gamma gene rearrangement, did not correlate with the presence of circulating Sezary cells or the increased risk of neoplasia. Our results indicate that circulating Sezary cells may be monoclonal (neoplastic) or polyclonal (reactive), as defined by TCR gene rearrangement studies. Circulating Sezary cells in SS may be reactive in nature and not accurately reflect the actual tumor burden in the peripheral blood. The presence of circulating Sezary cells or the presence of a clone of cells defined by TCR-beta gene rearrangement in the peripheral blood is not limited to neoplastic disease processes.

Adult↗
PubMed1995

IL-12 reverses cytokine and immune abnormalities in Sezary syndrome.

Cutaneous T cell lymphoma is a lymphoproliferative disorder typically characterized by skin invasion of clonally derived malignant CD4+ lymphocytes that phenotypically resemble mature Th cells. Sezary syndrome (SzS) represents an advanced form of cutaneous T cell lymphoma associated with generalized erythroderma and involvement of the peripheral blood by the malignant cell population. We have previously demonstrated aberrant cytokine production by PBMC in SzS characterized by increased IL-4 and deficient IL-2 and IFN-gamma production, as well as increased expression of mRNA for IL-4 and IL-5 within active skin lesions, suggesting that the clonal T cell population is derived from the Th 2 subset of helper T lymphocytes. These findings have been associated with a constellation of immune abnormalities that have been attributed to the cytokine abnormalities. Because IL-12 is a potent inducer of IFN-gamma production, and causes the activation of cytotoxic lymphocytes, we examined the production of IL-12 by PBMC from SzS patients and whether IL-12 could alter the unfavorable cytokine balance typical of SzS and thus lead to correction of immune defects. Despite normal numbers of peripheral blood monocytes and normal TNF-alpha production, mean Staphyloccus aureus and LPS-induced IL-12 p40 and p70 production by SzS PBMC was significantly decreased compared with PBMC from normal controls. Mean IFN-gamma production by patient PBMC in response to PHA alone was depressed, but increased to levels comparable with normal after addition of 1 ng/ml IL-12. Pretreatment of PBMC for 24 h with IL-12, IFN-alpha, or both together resulted in a decrease in PHA-stimulated IL-4 production from a base line of 1818 pg/ml to 1520, 1350, and 1058 pg/ml, respectively. Lastly, culture of patient PBMC with IL-12 for 24 h also resulted in significant increases in NK activity against K562 cells. These results indicate that PBMC from patients with SzS manifest a defect in IL-12 production and that the cytokine abnormalities associated with SzS can be favorably altered by IL-12.

Cytokines↗
PubMed1995

De novo development of psoriatic plaques in patients receiving interferon alfa for treatment of erythrodermic cutaneous T-cell lymphoma.

Presumably because of its potent immunomodulatory activity, the use of interferon has led to the development of autoimmune disease in susceptible individuals. Because psoriasis is considered to be, in part, an autoimmune phenomenon, it is plausible that interferon may influence disease activity. We describe the development of psoriatic plaques in two patients without a history of this disease while they were receiving interferon alfa and extracorporeal photochemotherapy for erythrodermic cutaneous T-cell lymphoma. Paradoxically, in both patients the erythroderma resolved with subsequent de novo onset of psoriasis. This clinical sequence provides support for disparate immune mechanisms in the pathogenesis of these disorders, both of which are typified by lymphoid infiltrates. A review of the literature reveals that all forms of interferons have been associated with the exacerbation of psoriatic plaques, but that only interferon alfa has induced de novo development of psoriasis.

Adult↗
PubMed1995

Large-cell transformation following detection of minimal residual disease in cutaneous T-cell lymphoma: molecular and in situ analysis of a single neoplastic T-cell clone expressing the identical T-cell receptor.

PURPOSE: One of the unique characteristics of cutaneous T-cell lymphoma (CTCL) is its ability to undergo cytologic transformation in which the malignant T cells develop the morphologic appearance of a large-cell lymphoma. Reported to occur in up to 20% of advanced cases, large-cell transformation (LCT) is associated with an aggressive clinical course. Little is known about the risk factors or the molecular mechanisms of LCT. Before current immunohistochemical and molecular techniques, it was not possible to determine if LCT represented changes of the initial neoplastic T-cell clone or, in fact, was a distinct second malignancy. The goal of this study was to define the clonal evolution of LCT in CTCL. PATIENTS AND METHODS: Polymerase chain reaction (PCR) amplification of T-cell receptor-beta (TCR-beta) gene rearrangements and immunohistochemistry with monoclonal antibodies to TCR-V beta regions were used as markers of T-cell clonality to analyze the skin and peripheral blood of a patient with CTCL and LCT. RESULTS: We first detected the presence of minimal residual disease (MRD) in a CTCL patient with a complete clinical response to biologic response modifiers (BRMs). When clinical relapse occurred and demonstrated LCT, TCR-beta-PCR and in situ immunohistochemistry with a specific TCR-V beta monoclonal antibody identified a single neoplastic T-cell clone that expressed the identical TCR as the original clone. CONCLUSION: Our results confirm a common clonal origin for CTCL and LCT. We also provide evidence of MRD in CTCL by molecular analysis, implying that residual malignant cells maintain a potential for clinical relapse and possibly LCT. The role of MRD detection remains to be defined in the clinical assessment of CTCL. LCT in CTCL provides a unique model to investigate the molecular events that underlie terminal-stage tumor progression.

Amino Acid Sequence↗
PubMed1995

Mycosis fungoides palmaris et plantaris.

BACKGROUND: Mycosis fungoides primarily localized to the palms and soles is rare and has been previously reported as cutaneous lymphoma in four patients or as Woringer-Kolopp disease in eight patients. OBSERVATIONS: Four patients were initially diagnosed and treated unsuccessfully for various palmoplantar dermatitides until histopathologic findings revealed mycosis fungoides. Each case exhibited a clonal rearrangement of T-cell receptor gamma genes and immunohistochemical studies consonant with mycosis fungoides. All patients had limited skin involvement without evidence of extracutaneous involvement. CONCLUSIONS: Mycosis fungoides palmaris et plantaris is an uncommon expression of mycosis fungoides that manifests primarily on the palms and soles and clinically may mimic various inflammatory palmoplantar dermatoses. A biopsy is recommended in the evaluation of recalcitrant palmoplantar dermatoses.

Diagnosis, Differential↗
PubMed1994

Determination of the primary structures of human skin chymase and cathepsin G from cutaneous mast cells of urticaria pigmentosa lesions.

This study establishes the primary structure of human skin chymase and provides further evidence for the presence of a cathepsin G-like proteinase within human mast cells. The amino acid sequence of human skin chymase was established by protein methods and by analysis of PCR amplification products obtained with cDNA-derived from urticaria pigmentosa (UP) lesions. UP is a disease characterized by skin lesions containing high numbers of mast cells. Proteolytic digests of human chymase purified from normal skin yielded 10 resolvable peptides that were sequenced by automated Edman degradation. The amino acid sequences for these peptides combined with the sequence obtained for the protein's NH2-terminal region (35 residues) accounted for 137 residues of the human skin chymase sequence. This partial amino acid sequence corresponded to the sequence of human heart chymase, a proteinase isolated from heart tissue with immunologic and hydrolytic properties similar to skin chymase. PCR amplification of UP-derived cDNA with primers based on the cDNA structure of heart chymase demonstrated a single amplification product of expected size which was subcloned and sequenced. The amino acid sequence (135 residues) deduced from this product was identical to that of heart chymase in the region between the primers. This sequence, along with that established for the purified protein, constituted 99% of the heart chymase primary structure, strongly indicating that human skin and heart chymases have identical primary structures. Amplification of the same UP-cDNA with primers coding for the NH2- and COOH-terminal sequences of human neutrophil cathepsin G also produced a specific amplification product which was sequenced. The deduced amino acid sequence between the primers was identical to that reported for neutrophil cathepsin G, indicating that the protein of cutaneous mast cells previously shown to be immunologically cross-reactive with neutrophil cathepsin G has a comparable amino acid sequence. UP-cDNA demonstrating amplification products for cathepsin G did not demonstrate amplification products for human neutrophil elastase, suggesting that the cathepsin G PCR amplification product was not derived from neutrophils or monocytes possibly contaminating the lesion. These studies provide further evidence that human skin mast cells contain two different chymotrypsin-like proteinases.

Amino Acid Sequence↗