Immunotherapy for Infectious Diseases

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311 Table 4 Case Reports of Unusual Fungal Infections Treated with Growth Factors or Cytokines as Adjunctive Therapy Infection Predisposing conditions Therapy Outcome Ref. no. Blastoschizomyces capitis Neutropenia, myelosuppressive therapy for leukemia AmB and GM-CSF Cured (60) Disseminated Fusarium Neutropenia, myelosuppressive therapy for leukemia AmB, 5-FC, GM-CSF Remission (96) Cutaneous mucormycosis Neutropenia, aplastic anemia, bone marrow transplantation AmB, surgical debridement, Cured (97) (Absidia corymbifera) G-CSF Pulmonary mucormycosis Neutropenia, myelosuppressive therapy for leukemia AmB, 5-FC, miconazole, Cured (98) pneumonectomy, G-CSF Sinonasal mucormycosis Neutropenia, myelosuppressive therapy for lymphoma AmB, itraconazole, surgical Cured (99) (Scopulariopsis candida) debridement, G-CSF Paecilomyces varioti Chronic granulomatous disease AmB, itraconazole, IFN-� Cured (100,101) Pseudallescheria boydii Chronic granulomatous disease Miconazole, IFN-� Cured (53) Trichosporonosis Neutropenia, myelosuppressive therapy for leukemia AmB, G-CSF Cured (102) (Trichosporon beigelii) Trichosporonosis Neutropenia, myelosuppressive therapy for multiple AmB, G-CSF Died (103) (Trichosporon beigelii) myeloma Disseminated zygomycosis Aplastic anemia, cyclosporin, antithymocyte globulin AmB, G-CSF Remission (104) (Rhizomucor pusillus) Abbreviations: AmB, amphotericin B; 5-FC, 5-fluorocytosine; CSF, colony-stimulating factor; G, granulocyte; M, macrophage; IFN-�, interferon-�.
312 Casadevall There has been some concern that GM-CSF administration may impair PMN migration to sites of infection because of GM-CSF-mediated effects on neutrophil adhesion. However, clinical experience suggests that this concern may be unfounded. One case report measured migration of labeled white blood cells in a patient with fungal infection treated with GM-CSF and pentoxifylline and demonstrated their localization to the site of infection (40). A small retrospective study that analyzed the incidence of fungal infections in patients who had received GM-CSF and other cytokines suggested that GM-CSF had a protective role in bone marrow transplant patients (41). Another retrospective study of infectious disease complications in autologous bone marrow transplant patients suggested no deleterious effects of GM-CSF on host immune function (42). In fact, there was a significant reduction in the incidence of total infectious complications and days of amphotericin B therapy as well as a trend toward fewer fungal infections (42). Since the time to resolution of neutropenia did not differ in patients with and without GM-CSF therapy, these results were interpreted as suggesting that GM-CSF enhanced monocyte-macrophage function and that this reduced infections (42). GM-CSF has been used as an adjunct to amphotericin B therapy in a few patients. Bodey et al. (43) reported a pilot study in which GM-CSF was administered to eight patients with malignancy, severe neutropenia, and proven systemic fungal infection in doses ranging from 100 to 750 �g/m 2 /day. Of the eight patients, four were cured, two had a partial response, and two failed therapy (43). A capillary leak syndrome developed as an adverse effect in three of the eight patients, contributing to one death and resulting in renal failure in another patient, presumably because the dose of GM-CSF was excessive (43). In a small study conducted by the Eastern Cooperative Oncology Group, the overall mortality of patients with acute myeloid leukemia and fungal infection was 13% in the group receiving GM-CSF and 75% in the control group (44). Whether this reduction in mortality was a result of earlier bone marrow recovery or enhanced effector cell function is unclear (44). Although encouraging, such data are preliminary, derived from a relatively few patients, and must be interpreted with caution. M-CSF The effects of this growth factor are limited to monocytic cell populations. M-CSF promotes proliferation, activation, and differentiation of monocytes and macrophages. M-CSF stimulates macrophages to produce higher levels of oxidants and enhances their ability to kill intracellular bacteria and fungi. Because the macrophage is a central host effector cell for defense against most, if not all, fungal infections, M-CSF is of particular interest as an immunotherapeutic agent in fungal infections. Several studies have shown that M-CSF can enhance macrophage function against fungi (Table 3). Nemunaitis and collaborators (45,46) used M-CSF in doses ranging from 100 to 2000 �g/m 2 /day as an adjunct to antifungal therapy in 24 patients with bone marrow transplants complicated by invasive fungal infections. Of these patients, 25% resolved their infection, 50% could not be evaluated for judging the efficacy of the intervention, and 25% did not respond (45). In a larger follow-up study, bone marrow transplant patients with fungal infections treated with M-CSF and antifungal therapy had significantly improved longterm survival compared with historical controls treated with antifungal therapy alone (46). The results suggest that benefits of adjunctive M-CSF therapy occur primarily in the subset of patients with Candida infections (46). This encouraging study suggests the need for
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Immunotherapy for Infectious Diseas
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In f e c t i o u s . D i s e a s e
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© 2002 Humana Press Inc. 999 River
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vi Preface I am grateful to all of
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viii Contents 11 Passive Immunother
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x Contributors BARBARA G. MATTHEWS,
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From: Immunotherapy for Infectious
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Humoral Immunity 5 Fig. 1. Humoral
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Humoral Immunity 7 Table 1 Properti
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Humoral Immunity 9 minal complement
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Humoral Immunity 11 ficity. In ligh
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Humoral Immunity 13 Fig. 7. VDJ joi
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Humoral Immunity 15 Fig. 9. Messeng
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Humoral Immunity 17 In contrast to
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Humoral Immunity 19 advantage to tr
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Humoral Immunity 21 32. Allman DM,
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Some Basic Cellular Immunology Prin
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Cellular Immunology Principles 25 i
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Cellular Immunology Principles 27 s
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Cellular Immunology Principles 29 d
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Cellular Immunology Principles 31 f
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Cellular Immunology Principles 33 F
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Cellular Immunology Principles 35 R
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Cellular Immunology Principles 37 1
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INTRODUCTION Immune Defense at Muco
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Immune Defense at Mucosal Surfaces
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II Molecular Basis for Immunotherap
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64 Kunert and Katinger IMMUNOGLOBUL
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66 Fig. 2. Monomeric, dimeric, and
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68 Kunert and Katinger Fig. 4. Humo
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70 Kunert and Katinger remove prote
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72 Kunert and Katinger Fig. 6. Diff
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74 Kunert and Katinger persons of a
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76 Kunert and Katinger that so-call
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78 Kunert and Katinger whereas sele
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80 Kunert and Katinger Different pr
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82 Kunert and Katinger HUMAN/MOUSE
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84 Kunert and Katinger are expresse
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86 Kunert and Katinger missing meta
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88 Kunert and Katinger Fig. 8. Sche
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90 Kunert and Katinger include a se
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92 Kunert and Katinger 32. Lee S, e
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94 Kunert and Katinger 72. Abbs IC,
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96 Kunert and Katinger 117. Wright
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Dendritic Cells 101 several organis
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Dendritic Cells 103 tion that infec
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Dendritic Cells 105 chaperones such
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Dendritic Cells 107 CD8� CTLs, th
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Dendritic Cells 109 complete tumor
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Dendritic Cells 111 19. Holland SM,
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Dendritic Cells 113 mouse pneumonit
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Dendritic Cells 115 dendritic cells
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INTRODUCTION Cytokines, Cytokine An
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Cytokines, Cytokine Antagonists, an
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Principles of Vaccine Development F
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Principles of Vaccine Development 1
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INTRODUCTION Immunopathogenesis of
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Immunopathogenesis of HIV Disease 1
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164 Connick counts ranged from 73 t
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166 Connick retinitis in an individ
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168 Connick A novel method of ident
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170 Connick occurs quite early in i
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172 Connick 2. Delta Coordinating C
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174 Connick 39. Hurni MA, Bohlen L,
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176 Connick 76. Dolan M.J., Clerici
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178 Connick 114. Komanduri KV, Visw
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Active Immunization for HIV Infecti
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200 Jacobson changes of gp120 alter
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202 Jacobson is reduced (54,55). A
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204 Jacobson Table 2 Potential Prot
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206 Jacobson from the SIV/17E-Cl-in
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208 Jacobson Several groups have de
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210 Jacobson HUMAN STUDIES Polyclon
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212 Jacobson clinical isolates, whi
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214 Jacobson 22. Beasley RP, Hwang
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216 Jacobson 59. Yoshiyama H, Mo H,
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218 Jacobson 95. Prince AM, Reesink
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220 Jacobson 133. Stiehm ER, Lamber
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222 Kilby and Bucy Although clinica
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224 Kilby and Bucy can infect human
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226 Kilby and Bucy the proinflammat
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228 Kilby and Bucy CD3/CD28, and th
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230 Kilby and Bucy of viral replica
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232 Kilby and Bucy 21. Cao Y, Qin L
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234 Kilby and Bucy 64. Pantaleo G,
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236 Kilby and Bucy 101. Clements-Ma
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238 Dornburg and Pomerantz cells (5
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240 Dornburg and Pomerantz Fig. 2.
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242 Dornburg and Pomerantz domains
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244 Dornburg and Pomerantz GENETIC
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246 Dornburg and Pomerantz Fig. 5.
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248 Dornburg and Pomerantz 6. Balti
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Viral Infections Other than HIV 253
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Page 295 and 296: 284 Wallis and Johnson replication
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Page 307 and 308: 296 Wallis and Johnson 37. Boom WH.
Page 309 and 310: 298 Wallis and Johnson 77. Ellner J
Page 311 and 312: 300 Wallis and Johnson 113. Raad I,
Page 313 and 314: 302 Wallis and Johnson 154. Anonymo
Page 315 and 316: 304 Table 1 Major Fungal Infections
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Page 327 and 328: 316 Casadevall CONCLUSION AND FUTUR
Page 329 and 330: 318 Casadevall 16. Boutati EI, Anai
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Page 335 and 336: 324 Index Blastomycosis, see Fungal
Page 337 and 338: 326 Index C-type retrovirus vectors
Page 339 and 340: 328 Index K Klebsiella, intravenous
Page 341 and 342: 330 Index Vaccine Recombinant vecto
Page 343: Infectious Disease IMMUNOTHERAPY FO
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