NDLI: Resting CD8 T cells recognize β-galactosidase expressed in the immune-privileged retina and mediate autoimmune disease when activated

Content Provider	PubMed Central
Author	Mcpherson, Scott W. Yang, Jing Chan, Chi-chao Dou, Chunzhi Gregerson, Dale S.
Copyright Year	2003
Abstract	Although the expression of class II major histocompatibility complex (MHC) in retina is extremely low, it is an established fact that activated CD4 T cells, specific for retinal antigens (Ags), mediate experimental autoimmune uveoretinitis (EAU). Conversely, CD8 T cells have not been shown to recognize Ag in the retina. This study investigated whether retinal-specific Ags are detected by class I MHC-restricted CD8 T cells. Using a CD8 T-cell clone (β3) specific for an immunodominant epitope of β-galactosidase (β-gal), local Ag recognition was shown by transfer of activated β3 cells into β-gal transgenic (Tg) mice expressing β-gal in the retina (hi-arr-β-gal mice), or in the brain and eye (GFAP-β-gal mice). β-gal-positive photoreceptor cells were damaged in the retina of hi-arr-β-gal mice, and anterior segment disease was found in the eyes of GFAP-β-gal mice. Ag recognition by resting CD8 T cells was also evaluated. Recovery of 5(6)-carboxyfluorescein diacetate N-succinimidyl ester (CFSE)-labelled β3 cells from hi-arr-β-gal mice was slightly decreased compared to recovery from B10.A mice, while recovery from GFAP-β-gal mice was transiently increased. Conversely, recovery of CFSE− cells increased in hi-arr-β-gal mice, consistent with an Ag-dependent response. The CFSE content of the CFSE+ population was unchanged relative to β3 cells recovered from controls. Intracellular cytokine responses of β3 cells recovered from hi-arr-β-gal and GFAP-β-gal mice correlated with the number of cells recovered, regardless of CFSE content. Even though their production of interferon-γ and tumour necrosis factor-α was affected little by transfer into hi-arr-β-gal recipients, the ability of β3 cells to mediate delayed-type hypersesitivity was inhibited in hi-arr-β-gal mice. These results show that resting CD8 T cells are affected by the presence of Ag that originates in retina and, when activated prior to transfer, mediate pathogenic autoimmunity against retinal and other ocular targets.
Related Links	http://dx.doi.org/10.1046/j.1365-2567.2003.01750.x
Ending Page	396
Page Count	11
Starting Page	386
File Format	PDF
ISSN	00192805
e-ISSN	13652567
Journal	Immunology
Issue Number	3
Volume Number	110
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2003-11-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Immunology Immunology and Allergy Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Resting and activated T cells display different requirements for CD8 molecules

Inhibitory CD8+ T cells in Autoimmune Disease

Immune regulatory CNS-reactive CD8+ T cells in experimental autoimmune encephalomyelitis

Inducible immune regulation following autoimmune disease in the immune-privileged eye

CD80 Expressed by CD8+ T Cells Contributes to PD-L1-Induced Apoptosis of Activated CD8+ T Cells

Abortive activation precedes functional deletion of CD8+ T cells following encounter with self-antigens expressed by resting B cells in vivo

Tissue-Resident Exhausted Effector Memory CD8+ T Cells Accumulate in the Retina during Chronic Experimental Autoimmune Uveoretinitis

The Immune Privileged Retina Mediates an Alternative Activation of J774A.1 Cells

Antiviral CD8 T Cells Recognize Borna Disease Virus Antigen Transgenically Expressed in either Neurons or Astrocytes▿

Resting CD8 T cells recognize β-galactosidase expressed in the immune-privileged retina and mediate autoimmune disease when activated

Similar Documents

Resting and activated T cells display different requirements for CD8 molecules

Inhibitory CD8+ T cells in Autoimmune Disease

Immune regulatory CNS-reactive CD8+ T cells in experimental autoimmune encephalomyelitis

Inducible immune regulation following autoimmune disease in the immune-privileged eye

CD80 Expressed by CD8+ T Cells Contributes to PD-L1-Induced Apoptosis of Activated CD8+ T Cells

Abortive activation precedes functional deletion of CD8+ T cells following encounter with self-antigens expressed by resting B cells in vivo

Tissue-Resident Exhausted Effector Memory CD8+ T Cells Accumulate in the Retina during Chronic Experimental Autoimmune Uveoretinitis

The Immune Privileged Retina Mediates an Alternative Activation of J774A.1 Cells

Antiviral CD8 T Cells Recognize Borna Disease Virus Antigen Transgenically Expressed in either Neurons or Astrocytes▿

Resting CD8 T cells recognize β-galactosidase expressed in the immune-privileged retina and mediate autoimmune disease when activated