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Table 5 Role of NAbs in diseases

From: The immunology of B-1 cells: from development to aging

 

Disease/Model

 

Function

Ref.

Mice

Heart Disease

Atherosclerosis

Increased phagocytic uptake of oxLDL

[106]

Reduced inflammation and atherosclerotic lesions

[107,108,109,110]

Neurodegenerative diseases

Parkinson disease

Reduced neurodegeneration; improved synapse;Reduced motor dysfunction

[111]

Alzheimer’s disease

Reduced neurotoxic effect of amyloid plaques to cultured neurons from mice and rats

[112, 113]

Increased phagocytic uptake of plaques

[114,115,116]

Reduced amyloid plaque deposition

[117]

Organ injury and regeneration

Acute liver injury

Increased clearance of necrotic cell debris

[68]

IRI

Increased complement-induced injury

[100, 101, 118, 119]

Less organ injury and systemic inflammation

[99]

Hepatectomy

Increased liver regeneration after partial hepatectomy

[102]

Infectious diseases

Influenza

Increased viral neutralization

[103]

S. Pneumoniae

 Increased GM-CSGF release by recruited B1 cells

[120]

Candida albicans

Increased fungal neutralization 

[121]

Aspergillus fumigatus

[122]

Cryptococcus neoformans

[123, 124]

Influenza H1N1

Increased survival

[105]

Sepsis

Less systemic inflammation and improved survival

[125, 126]

Acinetobacter baumannii

Protection against infection

[127]

Malaria

Increased production of IL-3 and GM-CSF

[89]

Cancer

Melanoma, Breast cancer,Adenocarcinoma

Inhibition of tumor growth

[128]

Colon cancer

Inhibition growth of melanoma cells

[129]

Auto-immune diseases

Systemic lupus erythematosus

Reduced IgG-autoantibodies and autoimmune disease

[97]

Protection against lupus nephritis and (+) survival

[130,131,132]

Human

Cardiovascular diseases

Atherosclerosis

Reduced pathological uptake of oxLDL

[133]

Reduced atherosclerosis progression and LPC cytotoxicity

[134]

Neurodegenerative disease

Parkinson’s disease

Prevention of α-synuclein aggregation in vitro

[135, 136]

Alzheimer’s disease

Protective anti-Aβ antibodies in blood and CSF

[137, 138]

Less plaque burden

[139]

Lower cognitive decline

[140]

Cancer

Non-small cell lung carcinoma

Eliminates NeuGcGM3-expressing tumor cells in vitro

[141]

Lower anti- NeuGcGM3 responses in NSCLC patients

Epithelial cancer

Increased apoptosis of carcinoma cells in vitro

[142, 143]

Gastric cancer

Increased tumor-specific apoptosis

[144]

Auto-immune diseases

Systemic lupus erythematosus

Protection against lupus nephritis

[145]