| 1. |
- Adolfsson, Jörgen, et al.
(författare)
-
Upregulation of Flt3 expression within the bone marrow Lin(-)Sca1(+)c-kit(+) stem cell compartment is accompanied by loss of self-renewal capacity
- 2001
-
Ingår i: Immunity. - 1074-7613. ; 15:4, s. 659-669
-
Tidskriftsartikel (refereegranskat)abstract
- Flt3 has emerged as a potential regulator of hematopoietic stem cells (HSC). Sixty percent of cells in the mouse marrow Lin(-)Sca1(+)c-kit(+) HSC pool expressed flt3. Although single cell cloning showed comparable high proliferative, myeloid, B, and T cell potentials of Lin(-)Sca1(+)c-kit(+)flt3(+) and Lin(-)Sca1(+)c-kit(+)flt3(-) cells, only Lin(-)Sca1(+)c-kit(+)flt3(-) cells supported sustained multilineage reconstitution. In striking contrast, Lin(-)Sca1(+)c-kit(+)flt3(+) cells rapidly and efficiently reconstituted B and T lymphopoiesis, whereas myeloid reconstitution was exclusively short term. Unlike c-kit, activation of flt3 failed to support survival of HSC, whereas only flt3 mediated survival of Lin(-)Sca1(+)c-kit(+)flt3(+) reconstituting cells. Phenotypic and functional analysis support that Lin(-)Sca1(+)c-kit(+)flt3(+) cells are progenitors for the common lymphoid progenitor. Thus, upregulation of flt3 expression on Lin(-)Sca1(+)c-kit(+) HSC cells is accompanied by loss of self-renewal capacity but sustained lymphoid-restricted reconstitution potential.
|
|
| 2. |
- Brakebusch, Cord, et al.
(författare)
-
Beta1 integrin is not essential for hematopoiesis but is necessary for the T cell-dependent IgM antibody response.
- 2002
-
Ingår i: Immunity. - 1074-7613. ; 16:3, s. 465-477
-
Tidskriftsartikel (refereegranskat)abstract
- Several experimental evidences suggested that beta1 integrin-mediated adhesion of hematopoietic stem cells (HSC) is important for their function in the bone marrow (BM). Using induced deletion of the beta1 integrin gene restricted to the hematopoietic system, we show that beta1 integrin is not essential for HSC retention in the BM, hematopoiesis, and trafficking of lymphocytes. However, immunization with a T cell-dependent antigen resulted in virtually no IgM production and an increased secretion of IgG in mutant mice, while the response to a T cell-independent type 2 antigen showed decreases in both IgM and IgG. These data suggest that beta1 integrins are necessary for the primary IgM antibody response.
|
|
| 3. |
- Sitnicka Quinn, Ewa, et al.
(författare)
-
Key Role of flt3 Ligand in Regulation of the Common Lymphoid Progenitor but Not in Maintenance of the Hematopoietic Stem Cell Pool.
- 2002
-
Ingår i: Immunity. - 1074-7613. ; 17:4, s. 463-472
-
Tidskriftsartikel (refereegranskat)abstract
- The first lineage commitment step of hematopoietic stem cells (HSC) results in separation into distinct lymphoid and myeloid differentiation pathways, reflected in the generation of common lymphoid and myeloid progenitors (CLP and CMP, respectively). In this report we present the first evidence for a nonredundant regulator of this process, in that adult mice deficient in expression of the flt3 ligand (FL) have severely (10-fold) reduced levels of the CLP, accompanied by reductions in the earliest identifiable B and T cell progenitors. In contrast, CMP and HSC are unaffected in FL-deficient mice. Noteworthy, CLP express high levels of both the flt3 receptor and ligand, indicating a potential autocrine role of FL in regulation of the earliest lymphoid commitment step from HSC.
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
|
|
| 11. |
|
|
| 12. |
- Agace, William W., et al.
(författare)
-
Regionalized Development and Maintenance of the Intestinal Adaptive Immune Landscape
- 2017
-
Ingår i: Immunity. - : Elsevier BV. - 1074-7613. ; 46:4, s. 532-548
-
Forskningsöversikt (refereegranskat)abstract
- The intestinal immune system has the daunting task of protecting us from pathogenic insults while limiting inflammatory responses against the resident commensal microbiota and providing tolerance to food antigens. This role is particularly impressive when one considers the vast mucosal surface and changing landscape that the intestinal immune system must monitor. In this review, we highlight regional differences in the development and composition of the adaptive immune landscape of the intestine and the impact of local intrinsic and environmental factors that shape this process. To conclude, we review the evidence for a critical window of opportunity for early-life exposures that affect immune development and alter disease susceptibility later in life.
|
|
| 13. |
|
|
| 14. |
|
|
| 15. |
|
|
| 16. |
|
|
| 17. |
|
|
| 18. |
- Bernink, JH, et al.
(författare)
-
Human ILC1: To Be or Not to Be
- 2017
-
Ingår i: Immunity. - : Elsevier BV. - 1097-4180 .- 1074-7613. ; 46:5, s. 756-757
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
|
|
| 19. |
- Biram, Adi, et al.
(författare)
-
Bacterial infection disrupts established germinal center reactions through monocyte recruitment and impaired metabolic adaptation.
- 2022
-
Ingår i: Immunity. - : Elsevier BV. - 1097-4180 .- 1074-7613. ; 55:3
-
Tidskriftsartikel (refereegranskat)abstract
- Consecutive exposures to different pathogens are highly prevalent and often alter the host immune response. However, it remains unknown how a secondary bacterial infection affects an ongoing adaptive immune response elicited against primary invading pathogens. We demonstrated that recruitment of Sca-1+ monocytes into lymphoid organs during Salmonella Typhimurium (STm) infection disrupted pre-existing germinal center (GC) reactions. GC responses induced by influenza, plasmodium, or commensals deteriorated following STm infection. GC disruption was independent of the direct bacterial interactions with B cells and instead was induced through recruitment of CCR2-dependent Sca-1+ monocytes into the lymphoid organs. GC collapse was associated with impaired cellular respiration and was dependent on TNFα and IFNγ, the latter of which was essential for Sca-1+ monocyte differentiation. Monocyte recruitment and GC disruption also occurred during LPS-supplemented vaccination and Listeria monocytogenes infection. Thus, systemic activation of the innate immune response upon severe bacterial infection is induced at the expense of antibody-mediated immunity.
|
|
| 20. |
|
|
| 21. |
- Brodeur, SR, et al.
(författare)
-
C4b-binding protein (C4BP) activates B cells through the CD40 receptor
- 2003
-
Ingår i: Immunity. - 1074-7613. ; 18:6, s. 837-848
-
Tidskriftsartikel (refereegranskat)abstract
- We demonstrate that the a. chain of human C4b binding protein (C4BP) binds directly to CD40 on human B cells at a site that differs from that used by CD40 ligand. C4BP induces proliferation, upregulation of CD54 and CD86 expression, and IL4-dependent IgE isotype switching in normal B cells but not in B cells from patients with CD40 or IKKgamma/NEMO deficiencies. Furthermore, C4BP colocalized with B cells in the germinal centers of human tonsils. These observations suggest that C4BP is an activating ligand for CD40 and establish a novel interface between complement and B cell activation.
|
|
| 22. |
- Brodin, P, et al.
(författare)
-
A Call for Blood-In Human Immunology
- 2019
-
Ingår i: Immunity. - : Elsevier BV. - 1097-4180 .- 1074-7613. ; 50:6, s. 1335-1336
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
|
|
| 23. |
|
|
| 24. |
|
|
| 25. |
|
|
