Immunology Abstracts

Immunology ranks as one of the most rapidly expanding areas of biomedical science, covering topics from cancer and vaccine research to immune deficiencies and autoimmunity. Immunology Abstracts performs a vital function for scientists in this field by monitoring significant advances and bringing together diverse research results in one succinct journal. Studies relating to all aspects of immune systems in man and animals, in normal functions and disorders, are summarized. Concentrating on basic science research and its clinical implications. Researchers working in a wide range of biomedical fields will find information essential to their work summarized in this database.

Subject Coverage

Major areas of coverage include:

• Apoptosis
• Autoimmunity
• Complement
• Cytokines and chemokines
• Genetics
• Histocompatibility antigen systems
• Hypersensitivity
• Immune response against microorganisms
• Immunization (passive and active)
• Immunodeficiency and immunoproliferation
• Immunomodulation
• Immunopharmacology
• Inflammation
• Lymphoid organs, tissues, and cells
• Methodology
• Parasite immunology
• Reproductive immunology
• Transplantation
• Tumor immunology and immunotherapy

1982 - current

Monthly, with approximately 1,500 new records added

Over 336,945 records as of February 2007

Immunology Abstracts (1982 - 2003)

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TI:	Title IL-7 Is a Critical Factor in Modulating Lesion Development in Skn-Directed Autoimmunity
AU:	Author Staton, Pamela J; Carpenter, ABetts; Jackman, Susan H
AF:	Author Affiliation Departments of Microbiology, Immunology, and Molecular Genetics and Department of Pathology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25704
SO:	Source Journal of Immunology [J. Immunol.]. Vol. 176, no. 7, pp. 3978-3986. 1 Apr 2006.
IS:	ISSN 0022-1767
DE:	Descriptors Interleukin 7; Spleen; CD4 antigen; Autoimmunity; Lymphocytes T; Development; Adoptive transfer; Immunoregulation; Skin diseases; CD8 antigen; Animal models
AB:	Abstract In a murine model of autoimmunity targeted against the epidermal cell Ags, Skn, adoptive transfer of Skn-immune T cells to immunosuppressed recipients elicits skin lesions in areas of mild epidermal trauma. In this study, we examined peripheral regulation of Skn-induced autoreactivity disrupted by rendering the mice immunoincompetent. We found that regulation of Skn-directed autoimmunity was restored by cotransfer of normal syngeneic spleen cells at twice the concentration of Skn-immune cells and was evidenced by significantly reduced lesion severity by days 5-7 post-cotransfer compared with animals given injections of Skn-immune cells alone. Enrichment and depletion of normal CD4 super(+) or CD8 super(+) spleen cells and RT-PCR analysis of selected cytokines identified CD4 super(+) cells as the regulatory cells in the cotransfer inoculum; however, significant reduction in lesion severity was observed only when there was a concomitant increase in levels of IL-7. The role of IL-7 was further supported in that mice cotransferred with Skn-immune cells plus normal spleen cells, but also treated with anti-IL-7 Ab, no longer exhibited reduced lesion severity. To determine whether IL-7 expression without normal spleen cell cotransfer could modulate lesion development, an IL-7-encoding plasmid (pCMV-Tag1-IL-7) was topically delivered to sites flanking the stressed skin site in Skn-induced autoimmune mice. Daily application of 15 mu g of pCMV-Tag1-IL-7 significantly suppressed lesion severity. Our results support a mechanism for CD4 super(+) T cells and IL-7 in contributing to the control of autoreactivity.
LA:	Language English
SL:	Summary Language English
PY:	Publication Year 2006
PT:	Publication Type Journal Article
PB:	Publisher American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 USA,
CL:	Classification F 06360 Skin: Animal
UD:	Update 200604
SF:	Subfile Immunology Abstracts
AN:	Accession Number 6748692
PG:	Journal Pages 3978-3986
JV:	Journal Volume 176
JI:	Journal Issue 7

The following field codes are found in the records of this database. Here they are listed in alphabetical order by two-letter code.

AB = Abstract	LA = Language
AF = Author Affiliation	NT = Notes
AN = Accession Number	NU = Other Numbers
AU = Authors	OT = Original Title
CA = Corporate Author	PB = Publisher
CF = Conference	PT = Publication Type
CL = Classification Code	PY = Publication Year
DE = Descriptors	SF = Subfile Name
ED = Editor	SL = Summary Language
ER = Environmental Regime	SO = Source
IB = ISBN	TI = Title
ID = Identifiers	TR = ASFA Input Center Number
IS = ISSN	UD = Update