Skip to main content

Table 2 Comparison of adaptive immunity defects observed in the 3xTg-AD model and human AD

From: Peripheral adaptive immunity of the triple transgenic mouse model of Alzheimer’s disease

Immunologic modification 3xTg-AD mice AD patients
Hematopoietic stem cells Decreased bone marrow multipotent progenitorsa Reduced circulating CD34+ hematopoietic stem cells [18]
B lymphocytes Increased plasma cells in bone marrowa
Decreased in circulation [4]
Decreased in circulation [11, 72, 73]
B lymphocyte antibody secretion Increased IgGa Increased IgG [74]
T lymphocytes Decreased circulating helper (CD4) and cytotoxic (CD8) lymphocytes [4]
Increased Th17 polarizationa
Decreased [9, 14, 72, 73, 75]; no change [11, 74]
Increased circulating Th17 lymphocytes in early AD [47]
CD4+/CD8+ ratio Increased [4] Increased [14, 76]; no change [72, 73, 75]; decreased [9]
Plasma IL-1α concentration Decreased [59] Decreased [77, 78]; no change [75]
Other plasma cytokines Increased IL-2, IL-17 and GM-CSFa
Increased IL-12, decreased IL-1β, IL-5, IL-6, IL-17, TNF-α, IFN-γ, CCL2, CCL3, CCL5, CCL11, and GM-CSF [59]
Increased GM-CSF [76, 79]
Increased or no change in IL-1, IL-6, IL-10; Increased IL-4, Il-12, IL-16, Il-18; decreased, increased, or no change in TNF-α (for review see [80])
  1. 3xTg-AD triple-transgenic mouse model of Alzheimer’s disease, AD Alzheimer’s disease, IgG immunoglobulin G; GM-CSF granulocyte-macrophage colony-stimulating factor, IL interleukin
  2. aCurrent paper