Viruses and bone marrow failure

Rosenfeld, Stephen J.; Young, Neal S.

doi:10.1016/0268-960x(91)90037-d

Cited by 61 publications

(39 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite the many clinical and experimental observations showing hematopoietic abnormalities associated with infections [26][27][28][29], most studies have focused on documenting pathogen-induced effects on myeloid and erythroid lineages. Surprisingly, there are few reports on alterations in BM lymphocytes during infection [25,30].…”

Section: Discussionmentioning

confidence: 99%

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

et al. 2005

View full text Add to dashboard Cite

The ability of a microorganism to elicit or evade B cell responses represents a determinant factor for the final outcome of an infection. Although pathogens may subvert humoral responses at different stages of B cell development, most studies addressing the impact of an infection on the B cell compartment have focused on mature B cells within peripheral lymphoid organs. Herein, we report that a protozoan infection, i.e. a Trypanosoma cruzi infection, induces a marked loss of immature B cells in the BM, which also compromises recently emigrated B cells in the periphery. The depletion of BM immature B cells is associated with an increased rate of apoptosis mediated by a parasite-indirect mechanism in a Fas/FasL-independent fashion. Finally, we demonstrated that myeloid cells play an important role in B cell depletion, since CD11b + BM cells from infected mice secrete a product of the cyclooxygenase pathway that eliminates immature B cells. These results highlight a previously unrecognized maneuver used by a protozoan parasite to disable B cell generation, limiting host defense and favoring its chronic establishment.

show abstract

Section: Discussionmentioning

confidence: 99%

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

et al. 2005

View full text Add to dashboard Cite

show abstract

“…57 Isolated thrombocytopenia has also been observed during CMV infection. 58 CMV modulates various aspects of immune response, and different mechanisms of marrow suppression have been proposed, such as direct infection of hematopoietic progenitors or stromal cells, abnormal gene expression, and immune reaction against the infected cells. [59][60][61][62] More recent studies in longterm bone marrow cultures indicate that BMSC are targets of CMV infection and that CMV replicates in BMSCs.…”

Section: Immune-mediated Thrombocytopeniamentioning

confidence: 99%

Thrombocytopenia and hemostatic disorders in chronic graft versus host disease

Pulanić

Lozier

Pavletić

2009

Bone Marrow Transplant

View full text Add to dashboard Cite

“…The majority of studies to date have focused on the suppressive effects of viruses on bone marrow (BM) erythroid, myeloid and megakaryocyte lineage cells and the resulting peripheral consequences such as anemia or cytopenia [1]. A variety of mechanisms have been proposed to contribute to the suppression of hematopoiesis associated with different virus infections.…”

Section: Introductionmentioning

confidence: 99%

“…Despite the well-documented clinical effects of virusinduced BM suppression on erythroid and myeloid cells [1], the effects of virus infections on BM B lineage cells are to a large extent unknown. Using a murine model, we recently showed that influenza virus infection, which is known to cause lymphopenia in both birds and humans [10,11], has suppressive effects on early B cells in the BM, causing a transient severe depletion of BM B lineage cells in vivo [12].…”

Section: Introductionmentioning

confidence: 99%

Virus infection‐associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF‐α/LTα

et al. 2005

View full text Add to dashboard Cite

We previously showed that influenza virus infection of mice induces a depletion of bone marrow B lineage cells due to apoptosis of early B cells mediated by a mechanism involving TNF-a/LTa. Here we demonstrate that this effect is also observed with acute lymphocytic choriomeningitis virus (LCMV) infection and resulted in a deficiency of both splenic transitional B cells and mature follicular B cells. To determine whether there was an associated impairment of humoral immunity, we infected mice with LCMV and 10 days later at the peak of the B cell depletion, inoculated them with influenza virus. We found that influenza virus-specific antibody titers were dramatically reduced in mice recovering from LCMV infection compared to those in mice infected with influenza virus alone. Further, we showed that there was no reduction of the influenza virus-specific antibody response in LCMV-infected TNF-a/LTa-deficient mice, suggesting that TNF-a/LTa-mediated effects on bone marrow and/or peripheral lymphocytes were responsible for the observed impairment in humoral immunity. These results show that the TNF-a/LTa production induced following infection with diverse viruses has detrimental effects on early B cells in the bone marrow, and may be among the factors that lead to the severely compromised humoral immunity observed to subsequent heterologous infections.

show abstract

Viruses and bone marrow failure

Cited by 61 publications

References 61 publications

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

Thrombocytopenia and hemostatic disorders in chronic graft versus host disease

Virus infection‐associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF‐α/LTα

Contact Info

Product

Resources

About