Diabetes prone BB rats are severely deficient in natural killer T cells

Neal N. Iwakoshi; Dale L. Greiner; Aldo A. Rossini; John P. Mordes

doi:10.3109/08916939908993854

Diabetes prone BB rats are severely deficient in natural killer T cells

Neal N. Iwakoshi
, Dale L. Greiner
, Aldo A. Rossini
, John P. Mordes

Research output: Contribution to journal › Article › peer-review

36 Scopus citations

Abstract

Diabetes prone (DP) BB rats develop spontaneous autoimmune hyperglycemia. Coisogenic diabetes resistant (DR) BB rats develop diabetes in response to immunological and environmental perturbants, but not spontaneously. Both are used to model human insulin-dependent diabetes mellitus (IDDM). Deficiencies in natural killer (NK) T cells have been implicated in the expression of human IDDM, but little is known of their phenotype or function in the rat. We now report that the phenotype of NK T cells in the rat is αβTcR⁺CD8⁺CD4^-, comparable to the NK T cell phenotype reported for humans, which is αβTcR⁺CD4^-Vα24-JαQ, and either CD8^- or CD8αα⁺. We also report that DP- but not DR-BB rats are severely deficient in splenic and intrahepatic NKR-P1⁺ αβTcR⁺ (NK T) cells. Because RT6⁺ T cells are deficient in DP-BB rats, and because depletion of cells expressing RT6 induces IDDM in DR-BB rats, we studied NK T cells for expression of this antigen. We observed that the majority of rat NK T cells express RT6. In addition, injection of cytotoxic anti-RT6.1 monoclonal antibody depleted splenic and intrahepatic RT6⁺ NK T cells, T cells, and NK cells, but left intact the RT6^- subset of each population. These results suggest that deficiencies in NK T cells may play a role in the susceptibility of DP- and DR-BB rats, respectively, to spontaneous and induced autoimmune IDDM.

Original language	English (US)
Pages (from-to)	1-14
Number of pages	14
Journal	Autoimmunity
Volume	31
Issue number	1
DOIs	https://doi.org/10.3109/08916939908993854
State	Published - 1999
Externally published	Yes

Bibliographical note

Funding Information:
We thank Jean Leif and Kelly Lake for technical assistance. This work was supported in part by grants DK25306 (AAR), DK36024 (DLG), DK41235 (JPM), A107439 (Immunology Training Grant, NI) from the National Institutes of Health, an institutional Diabetes and Endocrinology Research Center Grant from the National Institutes of Health, and by Research Grants from the Juvenile Diabetes Fo u nd at i o n In t erna t ion a 1 (A A R ) . TI1 e contents of this publication are solely the respon-qibility of the authors and do not necessarily represent the official views of the National Institutes of Health.

Keywords

Autoimmunity
BB rat
Diabetes
Intrahepatic lymphocytes
NK T cell

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "Diabetes prone BB rats are severely deficient in natural killer T cells",

abstract = "Diabetes prone (DP) BB rats develop spontaneous autoimmune hyperglycemia. Coisogenic diabetes resistant (DR) BB rats develop diabetes in response to immunological and environmental perturbants, but not spontaneously. Both are used to model human insulin-dependent diabetes mellitus (IDDM). Deficiencies in natural killer (NK) T cells have been implicated in the expression of human IDDM, but little is known of their phenotype or function in the rat. We now report that the phenotype of NK T cells in the rat is αβTcR+CD8+CD4-, comparable to the NK T cell phenotype reported for humans, which is αβTcR+CD4-Vα24-JαQ, and either CD8- or CD8αα+. We also report that DP- but not DR-BB rats are severely deficient in splenic and intrahepatic NKR-P1+ αβTcR+ (NK T) cells. Because RT6+ T cells are deficient in DP-BB rats, and because depletion of cells expressing RT6 induces IDDM in DR-BB rats, we studied NK T cells for expression of this antigen. We observed that the majority of rat NK T cells express RT6. In addition, injection of cytotoxic anti-RT6.1 monoclonal antibody depleted splenic and intrahepatic RT6+ NK T cells, T cells, and NK cells, but left intact the RT6- subset of each population. These results suggest that deficiencies in NK T cells may play a role in the susceptibility of DP- and DR-BB rats, respectively, to spontaneous and induced autoimmune IDDM.",

keywords = "Autoimmunity, BB rat, Diabetes, Intrahepatic lymphocytes, NK T cell",

author = "Iwakoshi, \{Neal N.\} and Greiner, \{Dale L.\} and Rossini, \{Aldo A.\} and Mordes, \{John P.\}",

note = "Funding Information: We thank Jean Leif and Kelly Lake for technical assistance. This work was supported in part by grants DK25306 (AAR), DK36024 (DLG), DK41235 (JPM), A107439 (Immunology Training Grant, NI) from the National Institutes of Health, an institutional Diabetes and Endocrinology Research Center Grant from the National Institutes of Health, and by Research Grants from the Juvenile Diabetes Fo u nd at i o n In t erna t ion a 1 (A A R ) . TI1 e contents of this publication are solely the respon-qibility of the authors and do not necessarily represent the official views of the National Institutes of Health.",

year = "1999",

doi = "10.3109/08916939908993854",

language = "English (US)",

volume = "31",

pages = "1--14",

journal = "Autoimmunity",

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T1 - Diabetes prone BB rats are severely deficient in natural killer T cells

AU - Iwakoshi, Neal N.

AU - Greiner, Dale L.

AU - Rossini, Aldo A.

AU - Mordes, John P.

N1 - Funding Information: We thank Jean Leif and Kelly Lake for technical assistance. This work was supported in part by grants DK25306 (AAR), DK36024 (DLG), DK41235 (JPM), A107439 (Immunology Training Grant, NI) from the National Institutes of Health, an institutional Diabetes and Endocrinology Research Center Grant from the National Institutes of Health, and by Research Grants from the Juvenile Diabetes Fo u nd at i o n In t erna t ion a 1 (A A R ) . TI1 e contents of this publication are solely the respon-qibility of the authors and do not necessarily represent the official views of the National Institutes of Health.

PY - 1999

Y1 - 1999

N2 - Diabetes prone (DP) BB rats develop spontaneous autoimmune hyperglycemia. Coisogenic diabetes resistant (DR) BB rats develop diabetes in response to immunological and environmental perturbants, but not spontaneously. Both are used to model human insulin-dependent diabetes mellitus (IDDM). Deficiencies in natural killer (NK) T cells have been implicated in the expression of human IDDM, but little is known of their phenotype or function in the rat. We now report that the phenotype of NK T cells in the rat is αβTcR+CD8+CD4-, comparable to the NK T cell phenotype reported for humans, which is αβTcR+CD4-Vα24-JαQ, and either CD8- or CD8αα+. We also report that DP- but not DR-BB rats are severely deficient in splenic and intrahepatic NKR-P1+ αβTcR+ (NK T) cells. Because RT6+ T cells are deficient in DP-BB rats, and because depletion of cells expressing RT6 induces IDDM in DR-BB rats, we studied NK T cells for expression of this antigen. We observed that the majority of rat NK T cells express RT6. In addition, injection of cytotoxic anti-RT6.1 monoclonal antibody depleted splenic and intrahepatic RT6+ NK T cells, T cells, and NK cells, but left intact the RT6- subset of each population. These results suggest that deficiencies in NK T cells may play a role in the susceptibility of DP- and DR-BB rats, respectively, to spontaneous and induced autoimmune IDDM.

AB - Diabetes prone (DP) BB rats develop spontaneous autoimmune hyperglycemia. Coisogenic diabetes resistant (DR) BB rats develop diabetes in response to immunological and environmental perturbants, but not spontaneously. Both are used to model human insulin-dependent diabetes mellitus (IDDM). Deficiencies in natural killer (NK) T cells have been implicated in the expression of human IDDM, but little is known of their phenotype or function in the rat. We now report that the phenotype of NK T cells in the rat is αβTcR+CD8+CD4-, comparable to the NK T cell phenotype reported for humans, which is αβTcR+CD4-Vα24-JαQ, and either CD8- or CD8αα+. We also report that DP- but not DR-BB rats are severely deficient in splenic and intrahepatic NKR-P1+ αβTcR+ (NK T) cells. Because RT6+ T cells are deficient in DP-BB rats, and because depletion of cells expressing RT6 induces IDDM in DR-BB rats, we studied NK T cells for expression of this antigen. We observed that the majority of rat NK T cells express RT6. In addition, injection of cytotoxic anti-RT6.1 monoclonal antibody depleted splenic and intrahepatic RT6+ NK T cells, T cells, and NK cells, but left intact the RT6- subset of each population. These results suggest that deficiencies in NK T cells may play a role in the susceptibility of DP- and DR-BB rats, respectively, to spontaneous and induced autoimmune IDDM.

KW - Autoimmunity

KW - BB rat

KW - Diabetes

KW - Intrahepatic lymphocytes

KW - NK T cell

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U2 - 10.3109/08916939908993854

DO - 10.3109/08916939908993854

M3 - Article

C2 - 10593564

AN - SCOPUS:0033278096

SN - 0891-6934

VL - 31

SP - 1

EP - 14

JO - Autoimmunity

JF - Autoimmunity

IS - 1

ER -

Diabetes prone BB rats are severely deficient in natural killer T cells

Abstract

Bibliographical note

Keywords

UN SDGs

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