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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