Table 1.
Antigen-independent systemic effects of pro-inflammatory molecules produced by virus-infected tissue.
Cytokine | Target Organ | Effect |
---|---|---|
Type I IFN | Bone marrow | •Anti-viral conditioning of leukocytes [9] •HSC enter the cell cycle [19] |
Lymph node and spleen | •Expression of Granzyme B on memory T cells [33] •Expression of activation markers on T and B cells [25-29] |
|
CNS | •Fever, sickness [44-46] | |
IL-6 | Bone marrow | •Granulopoiesis [47] |
Spleen and lymph nodes | •CD4+ T cell proliferation and activation [48] | |
CNS | •Fever, sickness [46] | |
TNFa | Bone marrow | •Depletion of B cell precursors [35] |
CNS | •Fever, sickness [15] | |
IL-1β | CNS | •Fever, sickness [45,46] |
LT-α | Bone marrow | •Depletion of B cell precursors [35] |
GM-CSF, G-CSF, M-CSF | Bone marrow | •Granulopoiesis [49] •HSC mobilization [50] •Neutrophil activation [51] |
CCL-2, CCL-7 | Bone marrow | •Monocyte mobilization [37,38] |
CXCL1, CCL-3, CXCL10, CCL5, IL-1α, IFNλ, IL12, etc. | Systemic effects during virus infection remain to be defined |