Lymphocyte-mediated cytotoxicity

Annual Review of Immunology

Volumn 20, Issue , 2002, Pages 323-370

  Russell, John H ^a   Ley, Timothy J ^a  

^a MO   (United States)

Author keywords

Apoptosis; Fas; Granule exocytosis; Granzymes; Perforin

Indexed keywords

DIPEPTIDYL PEPTIDASE I; DNA FRAGMENT; FAS ANTIGEN; FAS LIGAND; GRANZYME A; GRANZYME B; PERFORIN;

APOPTOSIS; AUTOIMMUNE DISEASE; CELL KILLING; CELL MEDIATED CYTOTOXICITY; CLINICAL PATHWAY; CYTOTOXIC T LYMPHOCYTE; ENZYME ACTIVATION; EXOCYTOSIS; GRAFT VERSUS HOST REACTION; GRANULE CELL; HUMAN; INFECTION SENSITIVITY; LYMPHOCYTE; NATURAL KILLER CELL; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; REVIEW; T LYMPHOCYTE ACTIVATION; TARGET CELL; TUMOR CELL;

ADAPTOR PROTEINS, SIGNAL TRANSDUCING; ANIMALS; AUTOIMMUNE DISEASES; CARRIER PROTEINS; CYTOTOXICITY, IMMUNOLOGIC; EXOCYTOSIS; FAS-ASSOCIATED DEATH DOMAIN PROTEIN; GRAFT VS HOST REACTION; GRAFT VS LEUKEMIA EFFECT; GRANZYMES; HUMANS; LYMPHOCYTES; MEMBRANE GLYCOPROTEINS; MICE; PORE FORMING CYTOTOXIC PROTEINS; SERINE ENDOPEPTIDASES; SIGNAL TRANSDUCTION; VIRUS DISEASES;

EID: 0036217977     PISSN: 07320582     EISSN: None     Source Type: Book Series    
DOI: 10.1146/annurev.immunol.20.100201.131730     Document Type: Review

References (268)

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2. Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity
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4. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand
5. Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice
6. Experimental necrobiosis - A venture in cytobiology
7. Mechanisms of immune lysis. I. Physiological distinction between target cell death mediated by cytotoxic T lymphocytes and antibody plus complement
8. Mechanisms of immune lysis. II. CTL-induced nuclear disintegration of the target begins within minutes of cell contact
9. Cytotoxic T lymphocytes induce different types of DNA damage in target cells of different origins
10. FADD is required for DR4- and DR5-mediated apoptosis: Lack of trail-induced apoptosis in FADD-deficient mouse embryonic fibroblasts
11. TRAIL receptor-2 signals apoptosis through FADD and caspase-8
12. FADD/MORT1 and caspase-8 are recruited to TRAIL receptors 1 and 2 and are essential for apoptosis mediated by TRAIL receptor 2
13. Apo2L/TRAIL-dependent recruitment of endogenous FADD and caspase-8 to death receptors 4 and 5
14. Accessing complexity: The dynamics of virus-specific T cell responses
15. The functional loss of human natural killer cell activity induced by K562 is reversible via an interleukin-2-dependent mechanism
16. The reorientation of the Golgi apparatus and the microtubule-organizing center in the cytotoxic effector cell is a prerequisite in the lysis of bound target cells
17. Isolation and biochemical and functional characterization of perforin 1 from cytolytic T-cell granules
18. T cell growth cytokines cause the superinduction of molecules mediating antigen-induced T lymphocyte death
19. + cytotoxic T cells
20. IL-12 enhances IL-2 function by inducing CD25 expression through a p38 mitogen-activated protein kinase pathway
21. + T helper 1 effectors
22. + CTL that utilizes a perforin- rather than a Fas ligand-dependent cytotoxic mechanism
23. + CTL directed against herpes simplex virus-infected cells
24. Acute rejection of vascular heart allografts by perforin-deficient mice
25. Perforin/granzyme-dependent and -independent mechanisms are both important for the development of graft-versus-host disease after murine bone marrow transplantation
26. Perforin dependence of natural killer cell-mediated tumor control in vivo
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29. The central effectors of cell death in the immune system
30. Antiviral protection by virus-immune cytotoxic T cells: Infected target cells are lysed before infectious virus progeny is assembled
31. + T cells clear influenza virus by perforin or fas-dependent processes
32. Contributions of Fas-Fas ligand interactions to the pathogenesis of mouse hepatitis virus in the central nervous system
33. IFN-gamma is required for viral clearance from central nervous system oligodendroglia
34. Mouse hepatitis virus is cleared from the central nervous systems of mice lacking perforin-mediated cytolysis
35. The roles of perforin- and Fas-dependent cytotoxicity in protection against cytopathic and noncytopathic viruses
36. Perforin is essential for control of ectromelia virus but not related poxviruses in mice
37. Perforin pathway is essential for protection of mice against lethal ocular HSV-1 challenge but not corneal scarring
38. Pathogenesis of herpes simplex virus type 1-induced corneal inflammation in perforin-deficient mice
39. Tumor necrosis factor alpha plays a central role in immune-mediated clearance of adenoviral vectors
40. Crucial role of 55-kilodalton TNF receptor in TNF-induced adhesion molecule expression and leukocyte organ infiltration
41. + T cell-mediated protection against an intracellular bacterium by perforin-dependent cytotoxicity
42. Fas (CD95)-dependent cell-mediated immunity to Listeria monocytogenes
43. Endogenous tumor necrosis factor (cachectin) is essential to host resistance against Listeria monocytogenes infection
44. + T cells derived from TNF-deficient and TNF/perforin double-deficient mice
45. Comparative modeling of amoebapores and granulysin based on the NK-lysin structure-structural and functional implications
46. Processing, subcellular localization, and function of 519 (granulysin), a human late T cell activation molecule with homology to small, lytic, granule proteins
47. Granulysin-induced apoptosis. I. Involvement of at least two distinct pathways
48. An antimicrobial activity of cytolytic T cells mediated by granulysin
49. T-cell release of granulysin contributes to host defense in leprosy
50. Granulysin, a T cell product, kills bacteria by altering membrane permeability
51. Aberrant transcription caused by the insertion of an early transposable element in an intron of the Fas antigen gene of lpr mice
52. + T cells
53. Protection against Fas-dependent Th1-mediated apoptosis by antigen receptor engagement in B cells
54. The Fas/Fas ligand pathway and Bcl-2 regulate T cell responses to model self and foreign antigens
55. Autoimmune gld mutation uncouples suicide and cytokine/proliferation pathways in activated, mature T cells
56. The fas antigen is involved in peripheral but not thymic deletion of T lymphocytes in T cell receptor transgenic mice
57. Functional roles of Fas and Bcl-2-regulated apoptosis of T lymphocytes
58. The role of cytotoxicity in lymphocyte homeostasis
59. Mutations in RAB27A cause Griscelli syndrome associated with haemophagocytic syndrome
60. Defective granule exocytosis in Rab27a-deficient lymphocytes from Ashen mice
61. Identification of the homologous beige and Chediak-Higashi syndrome genes
62. A role for perforin in downregulating T-cell responses during chronic viral infection
63. Enhanced antibody and cytokine responses to influenza viral antigens in perforin-deficient mice
64. Perforin protects against autoimmunity in lupus-prone mice
65. + T cells by perforin
66. Greatly accelerated lymphadenopathy and autoimmune disease in lpr mice lacking tumor necrosis factor receptor I
67. Induction of apoptosis in mature T cells by tumour necrosis factor
68. A crucial role for p80 TNF-R2 in amplifying p60 TNF-R1 apoptosis signals in T lymphocytes
69. TNF receptor 2-deficient CD8 T cells are resistant to Fas/Fas ligand-induced cell death
70. TNF receptor 1 (TNFR1) and CD95 are not required for T cell deletion after virus infection but contribute to peptide-induced deletion under limited conditions
71. Immune down-regulation and peripheral deletion of CD8 T cells does not require TNF receptor-ligand interactions nor CD95 (Fas, APO-1)
72. + T cell-mediated insulin-dependent diabetes mellitus
73. Development of insulitis without diabetes in transgenic mice lacking perforin-dependent cytotoxicity
74. The role of Fas in autoimmune diabetes
75. A mouse CD8 T cell-mediated acute autoimmune diabetes independent of the perforin and Fas cytotoxic pathways: Possible role of membrane TNF
76. Reduced incidence and delayed onset of diabetes in perforin-deficient nonobese diabetic mice
77. Significant role for Fas in the pathogenesis of autoimmune diabetes
78. In autoimmune diabetes the transition from benign to pernicious insulitis requires an islet cell response to tumor necrosis factor alpha
79. Coxsackievirus B3-induced myocarditis: Perforin exacerbates disease, but plays no detectable role in virus clearance
80. Interleukin 1 is processed and released during apoptosis
81. Myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis is chronic/relapsing in perforin knockout mice, but monophasic in Fas- and Fas ligand-deficient lpr and gld mice
82. Fas and Fas ligand enhance the pathogenesis of experimental allergic encephalomyelitis, but are not essential for immune privilege in the central nervous system
83. Fas- and FasL-deficient mice are resistant to induction of autoimmune encephalomyelitis
84. Fas has a crucial role in the progression of experimental autoimmune encephalomyelitis
85. Treatment of experimental encephalomyelitis with a novel chimeric fusion protein of myelin basic protein and proteolipid protein
86. Fas-mediated apoptosis in clinical remissions of relapsing experimental autoimmune encephalomyelitis
87. Genetic control of pathogenic mechanisms in autoimmune demyelinating disease
88. Differential roles of Fas ligand in spontaneous and actively induced autoimmune encephalomyelitis
89. Dual role for Fas ligand in the initiation of and recovery from experimental allergic encephalomyelitis
90. Perforin and granzyme A expression identifying cytolytic lymphocytes in rheumatoid arthritis
91. Perforin-secreting killer cell infiltration and expression of a 65-kD heat-shock protein in aortic tissue of patients with Takayasu's arteritis
92. Potential involvement of Fas and its ligand in the pathogenesis of Hashimoto's thyroiditis
93. T cell-mediated Fas-induced keratinocyte apoptosis plays a key pathogenetic role in eczematous dermatitis
94. Involvement of the CD95 (APO-1/Fas) receptor/ligand system in multiple sclerosis brain
95. Multiple sclerosis: Fas signaling in oligodendrocyte cell death
96. Technical note: Aberrant detection of cell surface Fas ligand with anti-peptide antibodies
97. Mechanism of lymphocyte-mediated cytotoxicity
98. How do cytotoxic lymphocytes kill their target cells?
99. A noncytotoxic mast cell tumor line exhibits potent IgE-dependent cytotoxicity after transfection with the cytolysin/perforin gene
100. Purified perforin induces target cell lysis but not DNA fragmentation
101. Purification of three cytotoxic lymphocyte granule serine proteases that induce apoptosis through distinct substrate and target cell interactions
102. A natural killer cell granule protein that induces DNA fragmentation and apoptosis
103. Cytotoxicity with target DNA breakdown by rat basophilic leukemia cells expressing both cytolysin and granzyme A
104. Synergistic roles of granzymes A and B in mediating target cell death by rat basophilic leukemia mast cell tumors also expressing cytolysin/perforin
105. How to induce involuntary suicide: The need for dipeptidyl peptidase I
106. Cytotoxic lymphocytes require granzyme B for the rapid induction of DNA fragmentation and apoptosis in allogeneic target cells
107. Natural killer and lymphokine-activated-killer cells require granzyme B for the rapid induction of DNA fragmentation and apoptosis in susceptible target cells
108. Human and murine cytotoxic T lymphocyte serine proteases: Subsite mapping with peptide thioester substrates and inhibition of enzyme activity and cytolysis by isocoumarins
109. Activation of the apoptotic protease CPP32 by cytotoxic T-cell-derived granzyme B
110. Proteolytic activation of the cell death protease Yama/CPP32 by granzyme B
111. Cleavage of CPP32 by granzyme B represents a critical role for granzyme B in the induction of target cell DNA fragmentation
112. Perforin: More than just an effector molecule
113. Activation of recombinant murine cytotoxic cell proteinase-1 requires deletion of an amino-terminal dipeptide
114. Generation of active myeloid and lymphoid granule serine proteases requires processing by the granule thiol protease dipeptidyl peptidase I
115. Expression of recombinant human granzyme B
116. Production of fully active recombinant murine granzyme B in yeast
117. Dipeptidyl peptidase I is required for the processing and activation of granzymes A and B in vivo
118. Granzymes A and B are targeted to the lytic granules of lymphocytes by the mannose-6-phosphate receptor
119. Protein sorting and secretion during CTL killing
120. Perforin is activated by a proteolytic cleavage during biosynthesis which reveals a phospholipid-binding C2 domain
121. Inactivation and proteolytic degradation of perforin within lytic granules upon neutralization of acidic pH
122. Functional defects of NK cells treated with chloroquine mimic the lytic defects observed in perforin-deficient mice
123. Apoptosis induced by granzyme B-glycosaminoglycan complexes: Implications for granule-mediated apoptosis in vivo
124. DFF45/ICAD can be directly processed by granzyme B during the induction of apoptosis
125. Perforin lytic activity is controlled by calreticulin
126. Degranulation plays an essential part in regulating cell surface expression of Fas ligand in T cells and natural killer cells
127. Granulysin: A novel antimicrobial peptide of cytolytic T lymphocytes and natural killer cells
128. A distinct pathway of cell-mediated apoptosis initiated by granulysin
129. Cytolytic T-cell cytotoxicity is mediated through perforin and fas lytic pathways
130. Mechanisms responsible for granzyme B-independent cytotoxicity
131. Identification of mutation in two major mRNA isoforms of the Chediak-Higashi syndrome
132. Identification and mutation analysis of the complete gene for Chediak-Higashi syndrome
133. Genetic defects in Chediak-Higashi syndrome and the beige mouse
134. Control of lytic function by mitogen-activated protein kinase/extracellular regulatory kinase 2 (ERK2) in a human natural killer cell line: Identification of perforin and granzyme B mobilization by functional ERK2
135. Direct tumor lysis by NK cells uses a Ras-independent mitogen-activated protein kinase signal pathway
136. Pivotal role of phosphoinositide-3 kinase in regulation of cytotoxicity in natural killer cells
137. Rab27a is required for regulated secretion in cytotoxic T lymphocytes
138. Cytosolic delivery of granzyme B by bacterial toxins: Evidence that endosomal disruption, in addition to transmembrane pore formation, is an important function of perforin
139. ++ dependent receptor molecule for lymphocyte perforin
140. Resistance of CTL to perforin-mediated lysis
141. Dependence of the lytic activity of the N-terminal domain of human perforin on membrane lipid composition. Implications for T-cell self-preservation
142. Interferon-γ-induced membrane PAF-receptor expression confers tumor cell susceptibility to NK perforin-dependent lysis
143. Impaired binding of perforin on the surface of tumor cells is a cause of target cell resistance against cytotoxic effector cells
144. Function of granule perforin and esterases in T cell-mediated reactions. Components required for delivery of molecules to target cells
145. New paradigm for lymphocyte granule-mediated cytotoxicity. Target cells bind and internalize granzyme B, but an endosomolytic agent is necessary for cytosolic delivery and subsequent apoptosis
146. Granzyme B (GraB) autonomously crosses the cell membrane and perforin initiates apoptosis and GraB nuclear localization
147. Entry and trafficking of granzyme B in target cells during granzyme B-perforin-mediated apoptosis
148. Nuclear transport of granzyme B (Fragmentin-2)
149. Localization of granzyme B in the nucleus
150. Perforin-dependent nuclear entry of granzyme B precedes apoptosis, and is not a consequence of nuclear membrane dysfunction
151. Nuclear targeting of the serine protease granzyme A (fragmentin-1)
152. Mannose 6-phosphate/insulin-like growth factor II receptor is a death receptor for granzyme B during cytotoxic T cell-induced apoptosis
153. Expression and purification of enzymatically active recombinant granzyme B in a baculovirus system
154. A combinatorial approach defines specificities of members of the caspase family and granzyme B
155. Definition and redesign of the extended substrate specificity of granzyme B
156. The structure of the proapoptotic protease granzyme B reveals the molecular determinants of its specificity
157. Crystal structure of the caspase activator human granzyme B, a proteinase highly specific for an Asp-P1 residue
158. The three-dimensional structure of human granzyme B compared to caspase-3, key mediators of cell death with cleavage specificity for aspartic acid in P1
159. ICE-LAP6, a novel member of the ICE/Ced-3 gene family, is activated by the cytotoxic T cell protease granzyme B
160. The cytotoxic cell protease granzyme B initiates apoptosis in a cell-free system by proteolytic processing and activation of the ICE/CED-3 family protease, CPP32, via a novel two-step mechanism
161. Activation of an interleukin 1 converting enzyme-dependent apoptosis pathway by granzyme B
162. Granule-mediated killing: Pathways for granzyme B-initiated apoptosis
163. Granzyme B mimics apical caspases
164. Target cell lysis by CTL granule exocytosis is independent of ICE/Ced-3 family proteases
165. Caspase dependence of target cell damage induced by cytotoxic lymphocytes
166. The target cell nucleus is not required for cell-mediated granzyme- or Fas-based cytotoxicity
167. Granzyme B short-circuits the need for caspase 8 activity during granule-mediated cytotoxic T-lymphocyte killing by directly cleaving Bid
168. Mitochondria-dependent and -independent regulation of granzyme B-induced apoptosis
169. Initiation of apoptosis by granzyme B requires direct cleavage of Bid, but not direct granzyme B-mediated caspase activation
170. DFF, a heterodimeric protein that functions downstream of caspase-3 to trigger DNA fragmentation during apoptosis
171. The 40-kDa subunit of DNA fragmentation factor induces DNA fragmentation and chromatin condensation during apoptosis
172. A caspase-activated DNase that degrades DNA during apoptosis and its inhibitor ICAD
173. Cleavage of CAD inhibitor in CAD activation and DNA degradation during apoptosis
174. Caspase-3 is the primary activator of apoptotic DNA fragmentation via DNA fragmentation factor-45/inhibitor of caspase-activated DNase inactivation
175. Resistance to DNA fragmentation and chromatin condensation in mice lacking the DNA fragmentation factor 45
176. DNA fragmentation factor 45-deficient cells are more resistant to apoptosis and exhibit different dying morphology than wild-type control cells
177. Direct cleavage of the human DNA fragmentation factor-45 by granzyme B induces caspase-activated DNase release and DNA fragmentation
178. Bcl-2 blocks degranulation but not fas-based cell-mediated cytotoxicity
179. Bcl-2 prevents apoptosis induced by perforin and granzyme B, but not that mediated by whole cytotoxic lymphocytes
180. Bcl-2 expression in target cells leads to functional inhibition of caspase-3 protease family in human NK and lymphokine-activated killer cell granule-mediated apoptosis
181. Bcl-2 blocks perforin-induced nuclear translocation of granzymes concomitant with protection against the nuclear events of apoptosis
182. Dependence of granzyme B-mediated cell death on a pathway regulated by Bcl-2 or its viral homolog, BHRF1
183. Granzyme B-mediated apoptosis proceeds predominantly through a Bcl-2-inhibitable mitochondrial pathway
184. Granzyme B-mediated cytochrome c release is regulated by the Bcl-2 family members Bid and Bax
185. Granzyme B induces Bid-mediated cytochrome c release and mitochondrial permeability transition
186. Granzyme B can cause mitochondrial depolarization and cell death in the absence of Bid, Bax, Bak or cytochrome c release
187. Granzyme B/perforin-mediated apoptosis of Jurkat cells results in cleavage of Poly(ADP-ribose polymerase to the 89-kDa apoptotic fragment and less abundant 64-kDa fragment
188. Granzyme B directly and efficiently cleaves several downstream caspase substrates: Implications for CTL-induced apoptosis
189. Filamin (280-kDa actin-binding protein) is a caspase substrate and is also cleaved directly by cytotoxic T lymphocyte protease granzyme B during apoptosis
190. Human granzyme B degrades aggrecan proteoglycan in matrix synthesized by chondrocytes
191. Granzymes A and B directly cleave lamins and disrupt the nuclear lamina during granule-mediated cytolysis
192. Cleavage by granzyme B is strongly predictive of autoantigen status: Implications for initiation of autoimmunity
193. Serine esterase in cytolytic T lymphocytes
194. Extracellular granzyme A, complexed to proteoglycans, is protected against inactivation by protease inhibitors
195. Granzyme A initiates an alternative pathway for granule-mediated apoptosis
196. Granzyme A binding to target cell proteins
197. Granzyme A released upon stimulation of cytotoxic T lymphocytes activates the thrombin receptor on neuronal cells and astrocytes
198. Granzyme A is an interleukin 1b-converting enzyme
199. Recombinant human granzyme A binds to two putative HLA-associated proteins and cleaves one of them
200. A role for heat shock protein 27 in CTL-mediated cell death
201. Induction of rapid histone degradation by the cytotoxic T lymphocyte protease granzyme A
202. Inhibition of CPP32-like proteases prevents granzyme B- and Fas-, but not granzyme A-based cytotoxicity exerted by CTL clones
203. Granzyme A loading induces rapid cytolysis and a novel form of DNA damage independently of caspase activation
204. Granzymes (lymphocyte serine proteases): Characterization with natural and synthetic substrates and inhibitors
205. A family of serine esterases in lytic granules of cytolytic T lymphocytes
206. The human cytotoxic T cell granule serine protease granzyme H has chymotrypsin-like (chymase) activity and is taken up into cytoplasmic vesicles reminiscent of granzyme B-containing endosomes
207. Residual cytotoxicity and granzyme K expression in granzyme A deficient cytotoxic lymphocytes
208. Long range disruption of gene expression by a PGK-neo cassette
209. A cluster of hematopoietic serine protease genes is found on the same chromosomal band as the human a/d T-cell receptor locus
210. Structure and expression of a cluster of human hematopoietic serine protease genes found on chromosome 14q11.2
211. Three human elastase-like genes coordinately expressed in the myelomonocyte lineage are organized as a single genetic locus on 19pter
212. The human Metase gene (GzmM): Structure, sequence, and close physical linkage to the serine protease gene cluster on 19p 13.3
213. The 5′ flanking region of the human granzyme H gene directs expression to T/natural killer cell progenitors and lymphokine-activated killer cells in transgenic mice
214. A null mutation in the perforin gene impairs cytolytic T lymphocyte and natural killer cell-mediated cytotoxicity
215. Two distinct pathways of specific killing revealed by perforin mutant cytotoxic lymphocytes
216. Immune function in mice lacking the perforin gene
217. The role of cell-mediated cytotoxicity in acute GVHD after MHC-matched allogeneic bone marrow transplantation in mice
218. Graft-versus-host disease-associated lymphoid hypoplasia and B cell dysfunction is dependent upon donor T cell-mediated Fas-ligand function, but not perforin function
219. Cytotoxic T cell deficient in both functional Fas ligand and perforin show residual cytolytic activity yet lose their capacity to induce lethal acute graft-versus-host disease
220. Abrogation of graft-versus-host disease following allotransplantation of cytotoxically deficient bone marrow across major histocompatibility barriers
221. + natural killer T cells with limited capacity for graft-versus-host disease induction due to interferon γ production
222. Graft-versus-leukemia effect and graft-versus-host disease can be differentiated by cytotoxic mechanisms in a murine model of allogeneic bone marrow transplantation
223. Granulocyte colony-stimulating factor-mobilized allogeneic stem cell transplantation maintains graft-versus-leukemia effects through a perforin-dependent pathway while preventing graft-versus-host disease
224. Differential use of Fas ligand and perforin cytotoxic pathways by donor T cells in graft-versus-host disease and graft-versus-leukemia effect
225. + T cells each can utilize a perforin-dependent pathway to mediate lethal graft-versus-host disease in major histocompatibility complex-disparate recipients
226. + donor T cells: Involvement of cytotoxic function by donor lymphocytes prior to GvHD pathogenesis
227. Involvement of donor T-cell cytotoxic effector mechanisms in preventing allogeneic marrow graft rejection
228. + T cell homeostasis by perforin and interferon-γ
229. Perforin/fas-ligand double deficiency is associated with macrophage expansion and severe pancreatitis
230. Perforin gene defects in familial hemophagocytic lymphohistiocytosis
231. Spectrum of perforin gene mutations in familial hemophagocytic lymphohistiocytosis
232. The role of granzyme B in murine models of acute graft-versus-host disease and graft rejection
233. Granzyme A-deficient mice retain potent cell-mediated cytotoxicity
234. Biological activities of granzyme K are conserved in the mouse and account for residual Z-Lys-SBzl activity in granzyme A-deficient mice
235. Granzyme A is critical for recovery of mice from infection with the natural cytopathic vital pathogen, ectromelia
236. Granzymes are the essential downstream effector molecules for the control of primary virus infections by cytolytic leukocytes
237. +) cell granules, restricts the spread of herpes simplex virus in the peripheral nervous sytems of experimentally infected mice
238. In vitro- and ex vivo-derived cytolytic leukocytes from granzyme A × B double knockout mice are defective in granule-mediated apoptosis but not lysis of target cells
239. Granzyme A and B-deficient killer lymphocytes are defective in eliciting DNA fragmentation but retain potent in vivo anti-tumor capacity
240. Dipeptidyl peptidase I is essential for activation of mast cell chymases, but not tryptases, in mice
241. An essential role for dipeptidyl peptidase I in the activation of neutrophil-associated serine proteases and antibody-mediated acute arthritis
242. Loss-of-function mutations in the cathepsin C gene result in peridontal disease and palmoplantar keratosis
243. Mutations of the cathepsin C gene are responsible for Papillon-Lefèvre syndrome
244. Papillon-Lefèvre syndrome: Mutations and polymorphisms in the cathepsin C gene
245. Haim-Munk syndrome and Papillon-Lefèvre syndrome are allelic mutations in cathepsin C
246. Localization of a gene for prepubertal periodontitis to chromosome 11q14 and identification of a cathepsin C gene mutation
247. The syndrome of palmar-plantar hyperkeratosis and premature periodontal destruction of the teeth
248. A major role for the Fas pathway in acute graft-versus-host disease
249. Differential use of FasL- and perforin-mediated cytolytic mechanisms by T-cell subsets involved in graft-versus-myeloid leukemia responses
250. Perforin-mediated cytotoxicity is critical for surveillance of spontaneous lymphoma
251. A cytosolic granzyme B inhibitor related to the viral apoptotic regulator cytokine response modifier A is present in cytotoxic lymphocytes
252. A new family of 10 murine ovalbumin serpins includes two homologs of proteinase inhibitor 8 and two homologs of the granzyme B inhibitor (proteinase inhibitor 9)
253. Selective regulation of apoptosis: The cytotoxic lymphocyte serpin proteinase inhibitor 9 protects against granzyme B-mediated apoptosis without perturbing the Fas cell death pathway
254. Nucleocytoplasmic distribution of the ovalbumin serpin PI-9 requires a nonconventional nuclear import pathway and the export factor Crm1
255. Blockade of the granzyme B/perforin pathway through overexpression of the serine protease inhibitor PI-9/SPI-6 constitutes a mechanism for immune escape by tumors
256. Granzyme B is inhibited by the cowpox virus serpin cytokine response modifier A
257. CrmA, a poxvirus-encoded serpin, inhibits cytotoxic T-lymphocyte-mediated apoptosis
258. Differential inhibition of the Fas- and granule-mediated cytolysis pathways by the orthpoxvirus cytokine response modifier A/SPI-2 and SPI-1 protein
259. Target protease specificity of the viral serpin CrmA
260. Specific inhibition of granzyme B by parainfluenza virus type 3
261. Adenovirus L4-100K assembly protein is a granzyme B-substrate that potently inhibits granzyme B-mediated cell death
262. + T cell cytotoxic effector function
263. Theiler's virus infection of perforin-deficient mice
264. Perforin-dependent neurologic injury in a viral model of multiple sclerosis
265. + T cells or perforin
266. Murine cytomegalovirus replication in salivary glands is controlled by both perforin and granzymes during acute infection
267. Apoptosis mediated by Fas but not tumor necrosis factor receptor 1 prevents chronic disease in mice infected with murine cytomegalovirus
268. Immunological control of murine gammaherpesvirus infection is independent of perforin