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Mice lacking expression of secondary lymphoid organ chemokine have defects in lymphocyte homing and dendritic cell localization.

Gunn MD, Kyuwa S, Tam C, Kakiuchi T, Matsuzawa A, Williams LT, Nakano H - J. Exp. Med. (1999)

Bottom Line: Secondary lymphoid organ chemokine (SLC) is expressed in high endothelial venules and in T cell zones of spleen and lymph nodes (LNs) and strongly attracts naive T cells.DC migration to LNs after contact sensitization is also substantially reduced.The plt mutation maps to the SLC locus; however, the sequence of SLC introns and exons in plt mice is normal.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular Research Institute, University of California San Francisco, San Francisco, California 94143, USA. michael.gunn@duke.edu

ABSTRACT
Secondary lymphoid organ chemokine (SLC) is expressed in high endothelial venules and in T cell zones of spleen and lymph nodes (LNs) and strongly attracts naive T cells. In mice homozygous for the paucity of lymph node T cell (plt) mutation, naive T cells fail to home to LNs or the lymphoid regions of spleen. Here we demonstrate that expression of SLC is undetectable in plt mice. In addition to the defect in T cell homing, we demonstrate that dendritic cells (DCs) fail to accumulate in spleen and LN T cell zones of plt mice. DC migration to LNs after contact sensitization is also substantially reduced. The physiologic significance of these abnormalities in plt mice is indicated by a markedly increased sensitivity to infection with murine hepatitis virus. The plt mutation maps to the SLC locus; however, the sequence of SLC introns and exons in plt mice is normal. These findings suggest that the abnormalities in plt mice are due to a genetic defect in the expression of SLC and that SLC mediates the entry of naive T cells and antigen-stimulated DCs into the T cell zones of secondary lymphoid organs.

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(A and B) Whole mounts of abdominal epidermis from +/+  (A) and plt (B) mice show normal numbers and distribution of DCs. Abdominal epidermis was separated from dermis and stained with anti–I-Ad  (reference 31). (C and D) The accumulation of activated DCs in splenic T  cell zones is decreased in plt mice. Spleens of +/+ (C) and plt (D) mice were  removed 6 h after intraperitoneal injection of LPS. Frozen sections were  prepared and stained for CD11c+ DCs (red) and B220+ B cells (brown).
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Figure 5: (A and B) Whole mounts of abdominal epidermis from +/+ (A) and plt (B) mice show normal numbers and distribution of DCs. Abdominal epidermis was separated from dermis and stained with anti–I-Ad (reference 31). (C and D) The accumulation of activated DCs in splenic T cell zones is decreased in plt mice. Spleens of +/+ (C) and plt (D) mice were removed 6 h after intraperitoneal injection of LPS. Frozen sections were prepared and stained for CD11c+ DCs (red) and B220+ B cells (brown).

Mentions: To determine if the decreased accumulation of DCs in the LNs of plt mice was secondary to a decreased number of resident skin DCs, abdominal epidermis of +/+ and plt mice was stained with anti–I-A (Fig. 5, A and B). There was no significant difference in the density, morphology, or distribution of I-A+ DCs in the epidermis of untreated plt and +/+ mice. The average number of I-A+ epidermal cells in +/+ mice was 14 ± 2.1 per high power field (HPF) compared with 15.5 ± 2.8 in plt mice.


Mice lacking expression of secondary lymphoid organ chemokine have defects in lymphocyte homing and dendritic cell localization.

Gunn MD, Kyuwa S, Tam C, Kakiuchi T, Matsuzawa A, Williams LT, Nakano H - J. Exp. Med. (1999)

(A and B) Whole mounts of abdominal epidermis from +/+  (A) and plt (B) mice show normal numbers and distribution of DCs. Abdominal epidermis was separated from dermis and stained with anti–I-Ad  (reference 31). (C and D) The accumulation of activated DCs in splenic T  cell zones is decreased in plt mice. Spleens of +/+ (C) and plt (D) mice were  removed 6 h after intraperitoneal injection of LPS. Frozen sections were  prepared and stained for CD11c+ DCs (red) and B220+ B cells (brown).
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2192914&req=5

Figure 5: (A and B) Whole mounts of abdominal epidermis from +/+ (A) and plt (B) mice show normal numbers and distribution of DCs. Abdominal epidermis was separated from dermis and stained with anti–I-Ad (reference 31). (C and D) The accumulation of activated DCs in splenic T cell zones is decreased in plt mice. Spleens of +/+ (C) and plt (D) mice were removed 6 h after intraperitoneal injection of LPS. Frozen sections were prepared and stained for CD11c+ DCs (red) and B220+ B cells (brown).
Mentions: To determine if the decreased accumulation of DCs in the LNs of plt mice was secondary to a decreased number of resident skin DCs, abdominal epidermis of +/+ and plt mice was stained with anti–I-A (Fig. 5, A and B). There was no significant difference in the density, morphology, or distribution of I-A+ DCs in the epidermis of untreated plt and +/+ mice. The average number of I-A+ epidermal cells in +/+ mice was 14 ± 2.1 per high power field (HPF) compared with 15.5 ± 2.8 in plt mice.

Bottom Line: Secondary lymphoid organ chemokine (SLC) is expressed in high endothelial venules and in T cell zones of spleen and lymph nodes (LNs) and strongly attracts naive T cells.DC migration to LNs after contact sensitization is also substantially reduced.The plt mutation maps to the SLC locus; however, the sequence of SLC introns and exons in plt mice is normal.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular Research Institute, University of California San Francisco, San Francisco, California 94143, USA. michael.gunn@duke.edu

ABSTRACT
Secondary lymphoid organ chemokine (SLC) is expressed in high endothelial venules and in T cell zones of spleen and lymph nodes (LNs) and strongly attracts naive T cells. In mice homozygous for the paucity of lymph node T cell (plt) mutation, naive T cells fail to home to LNs or the lymphoid regions of spleen. Here we demonstrate that expression of SLC is undetectable in plt mice. In addition to the defect in T cell homing, we demonstrate that dendritic cells (DCs) fail to accumulate in spleen and LN T cell zones of plt mice. DC migration to LNs after contact sensitization is also substantially reduced. The physiologic significance of these abnormalities in plt mice is indicated by a markedly increased sensitivity to infection with murine hepatitis virus. The plt mutation maps to the SLC locus; however, the sequence of SLC introns and exons in plt mice is normal. These findings suggest that the abnormalities in plt mice are due to a genetic defect in the expression of SLC and that SLC mediates the entry of naive T cells and antigen-stimulated DCs into the T cell zones of secondary lymphoid organs.

Show MeSH
Related in: MedlinePlus