Microwave Spectroscopy

Contains reports on four research projects.Joint Services Electronics Programs (U. S. Army, U. S. Navy, and U. S. Air Force) under Contract DA 36-039-AMC-03200(E

Microwave Spectroscopy

Contains research objectives and reports on four research projects.Signal Corps Contract DA36-039-sc-7489

Quantum Optics and Photonics

Contains table of contents for Part II, table of contents for Section 1, and reports on six research projects.Charles S. Draper Laboratories Contract DL-H-418468U.S. Air Force - Electronic Systems Division Contract F19628-89-K-0300U.S. Navy - Office of Naval Research Grant N0014-91-J-1808U.S. Air Force - Electronic Systems Division Contract F19628-89-K-003

Quantum Optics and Photonics

Contains reports on nine research projects.National Science Foundation (Grant PHY82-10369)Joint Services Electronics Program (Contract DAAG29-83-K-0003)U.S. Air Force - Office of Scientific Research (Contract F49620-82-C-0091)Litton Guidance and Control SystemNational Science Foundation (Grant PHY82-10369

Photonics

Contains reports on seven research projects.Air Force Rome Air Development Center (in collaboration with C.C. Leiby, Jr.)U.S. Air Force-Rome Air Development Center (Contract F19628-80-C-0077)National Science Foundation (Grant PHY79-09739)Joint Services Electronics Program (Contract DAAG29-80-C-0104)U.S. Air Force Geophysics Laboratory (Contract F19628-79-C-0082

Quantum Optics and Photonics

Contains table of contents for Part II, table of contents for Section 1 and reports on six research projects.U.S. Air Force - Electronic Systems Division Contract F19628-92-K-0013U.S. Navy - Office of Naval Research Grant N0014-91-J-1808Ballistic Missile Defense Organization Grant NG0921-94-C-0101MIT Plasma Fusion Cente

Quantum Optics and Photonics

Contains table of contents for Part II, table of contains for Section 1 and reports on three research projects.Charles Stark Draper LaboratoryJoint Services Electronics Program (Contract DAAL03-86-K-0002)National Science Foundation (Grant PHY 82-10369)U.S. Air Force - Office of Scientific Research (Contract F49620-82-C-0091)U.S. Air Force - Rome Air Development Cente

Quantum Optics and Photonics

Contains reports on seven research projects.U.S. Air Force Geophysics Laboratory (Contract F19628-70-C-0082)Joint Services Electronics Program (Contract DAAG29-83-K-0003)National Science Foundation (Grant PHY82-10369)U.S. Air Force - Rome Air Development Center (in collaboration with C.C. Leiby, Jr.)U.S. Air Force - Rome Air Development Center (Contract F19628-80-C-0077)U.S. Air Force - Office of Scientific Research (Contract F49620-82-C-0091

Microwave Spectroscopy

Contains reports on four research projects

Disease-associated Bias in T Helper Type 1 (Th1)/Th2 CD4+ T Cell Responses Against MAGE-6 in HLA-DRB1*0401+ Patients With Renal Cell Carcinoma or Melanoma

T helper type 1 (Th1)-type CD4+ antitumor T cell help appears critical to the induction and maintenance of antitumor cytotoxic T lymphocyte (CTL) responses in vivo. In contrast, Th2- or Th3/Tr-type CD4+ T cell responses may subvert Th1-type cell-mediated immunity, providing a microenvironment conducive to disease progression. We have recently identified helper T cell epitopes derived from the MAGE-6 gene product; a tumor-associated antigen expressed by most melanomas and renal cell carcinomas. In this study, we have assessed whether peripheral blood CD4+ T cells from human histocompatibility leukocyte antigens (HLA)-DRβ1*0401+ patients are Th1- or Th2-biased to MAGE-6 epitopes using interferon (IFN)-γ and interleukin (IL)-5 enzyme-linked immunospot assays, respectively. Strikingly, the vast majority of patients with active disease were highly-skewed toward Th2-type responses against MAGE-6–derived epitopes, regardless of their stage (stage I versus IV) of disease, but retained Th1-type responses against Epstein-Barr virus– or influenza-derived epitopes. In marked contrast, normal donors and cancer patients with no current evidence of disease tended to exhibit either mixed Th1/Th2 or strongly Th1-polarized responses to MAGE-6 peptides, respectively. CD4+ T cell secretion of IL-10 and transforming growth factor (TGF)-β1 against MAGE-6 peptides was not observed, suggesting that specific Th3/Tr-type CD4+ subsets were not common events in these patients. Our data suggest that immunotherapeutic approaches will likely have to overcome or complement systemic Th2-dominated, tumor-reactive CD4+ T cell responses to provide optimal clinical benefit