Fas (CD 95) and Fas-ligand (CD 95L)

Sources/Clones
Fas (CD 95) Alexis Corp., San Diego, California (SM1/17, SM1/1, SM1/23, APO1-3), Dako (APO-1, DX2) and Pharmingen (DX2, G254-274).
Fas-Ligand (CD 95L, Anti-Fas)
Immunotech (4A5, 4H9) and Pharmingen (NOK-1, NOK-2, G247-4).

Fixation/Preparation
Several of the antibodies (clones APO-1, DX2) are immunoreactive in fixed, paraffin-embedded tissue sections as well as frozen sections and cell preparations.

Background
Fas (CD 95) is a cell surface protein that belongs to the tumor necrosis factor family. Crosslinking of Fas and Fas-ligand (FasL) transduces signals, which culminate in apoptosis in sensitive cells. These proteins therefore have a role in the genesis of neoplasms and have been extensively studied in this context. Their expression in certain malignancies has been implicated as a possible key mechanism in the immune privilege of such tumors. FasL is also expressed in immunologically privileged sites in the nonneoplastic state. The induction of apoptosis by FasL in invading lymphocytes acts as a mechanism of immune-privilege and is important in preventing graft rejection. The placenta, another immune-privileged site, has also been shown to express high levels of FasL. The induction of apoptosis in lymphocytes by invading trophoblasts may account for the immune tolerance of the fetal semiallograft (Hunt et al, 1997; Bamberger et al, 1997; Uckan et al, 1997). Experimentally, FasL can be employed to induce apoptosis in Fas-bearing cells.

Applications
Fas and FasL expression have been studied in a wide variety of tissues and in other diseases besides neoplasms (Nonomura et al, 1996; Tachibana et al, 1996; Nichans et al, 1997; Muller et al, 1997; Hellquist et al, 1997). These include idiopathic pulmonary fibrosis (Kazufumi et al, 1997), human cancers following ionizing radiation (Sheard et al, 1997), Alzheimers' disease (De La Monte et al, 1997), chronic hepatitis (Luo et al, 1997), alveolar type II pneumocytes (Fine et al, 1997), colonic epithelial cells (Strater et al, 1997), inflammatory myopathies (Behrens et al, 1997), diabetes (Chervonsky et al, 1997) and germ cells of the testis (Lee et al, 1997).

References
•Bamberger AM, Schulte HM, Thuneke I et al 1997 Expression of the apoptosis-inducing Fas ligand (FasL) in human first and third trimester placenta and choriocarcinoma cells. Journal of Clinical Endocrinology and Metabolism 82: 3173-3175.

•Behrens L, Bender A, Johnson MA, Hohlfeld R 1997 Cytotoxic mechanisms in inflammatory myopathies. Co-expression of Fas and protective Bcl-2 in muscle fibres and inflammatory cells. Brain 120: 929-938. Chervonsky AV, Wang Y, Wong FS et al 1997 The role of Fas in autoimmune diabetes. Cell 89: 17-24.

•De La Monte SM, Sohn YK, Wands JR 1997 Correlates of p53- and Fas (CD95)-mediated apoptosis in Alzheimer's disease. Journal of Neurological Sciences 152: 73-83. Alzheimer's disease. Journal of Neurological Sciences 152: 73-83.

•Fine A, Anderson NL, Rothstein TL et al 1997 Fas expression in pulmonary alveolar type II cells. American Journal of Physiology 273: L64-L71.

•Hellquist HB, Olejnicka B, Jadner M et al 1997. Fas receptor is expressed in human lung squamous cell carcinomas, whereas bcl-2 and apoptosis are not pronounced: a preliminary report. British Journal of Cancer 76: 175-179.

•Hunt JS, Vassmer D, Ferguson TA, Miller L 1997. Fas ligand is positioned in mouse uterus and placenta to prevent trafficking of activated leukocytes between the mother and the conceptus. Journal of Immunology 158: 4122-4128.

•Kazufumi M, Sonoko N, Masanori K et al 1997 Expression of bcl-2 protein and APO-1 (Fas antigen) in the lung tissue from patients with idiopathic pulmonary fibrosis. Microscopy Research Technology 38: 480-487.

•Lee J, Richburg JH, Younkin SC, Bockelheide K 1997 The Fas system is a key regulator of germ cell apoptosis in the testis. Endocrinology 138: 2081-2088.

•Luo KX, Zhu YF, Zhang LX et al 1997 In situ investigation of Fas/FasL expression in chronic hepatitis B infection and related liver diseases. Journal of Viral Hepatitis 4: 303-307.

•Muller M, Strand S, Hug H, et al 1997 Drug-induced apoptosis in hepatoma cells is mediated by the CD95 (APO-1/Fas) receptor/ligand system and involves activation of wild-type p53. Journal of Clinical Investigation 99: 403-413.

•Nichans GA, Brunner T, Frizelle SP et al 1997. Human lung carcinomas express Fas ligand. Cancer Research 57: 1007-1012.

•Nonomura N, Miki T, Yokoyama M, et al 1996 Fas/APO-1-mediated apoptosis of human renal cell carcinoma. Biochemistry and Biophysiology Research Communications 229:945-951.

•Sheard MA, Vojtesek B, Janakova L et al 1997 Up-regulation of Fas (CD 95) in human p53 wild-type cancer cells treated with ionizing radiation. International Journal of Cancer 73: 757-762.

•Strater J, Wellisch I, Riedl S et al 1997. CD 95 (APO-1/Fas)-mediated apoptosis in colon epithelial cells: a possible role in ulcerative colitis. Gastroenterology 113: 160-167.

•Uckan D, Steele A, Wang BY et al 1997. Trophoblasts express Fas ligand: a proposed mechanism for immune privilege in placenta and maternal invasion. Molecular Human Reproduction 3: 655-662.

•Tachibana O, Lampe J, Kleihues P, Obgaki H 1996 Preferential expression of Fas/APO1 (CD95) and apoptotic cell death in perinecrotic cells of glioblastoma multiforme. Acta Neuropathologica (Berlin) 92: 431-434.

Bibliografía
Manual of diagnostic antibodies for immunohistology / Anthony S.-Y. Leong, Kumarasen Cooper, F. Joel W.-M. Leong.