1. |
Rheumatoid Arthritis (RA) |
Polymorphisms in FOXP3 gene associated
with reduced frequency of Treg, TGFβ and IL-10, in RA |
[29] |
|
|
Increased circulating HLA-DR+Tregs or
inflammation-associated Tregs which are suppressive but have similar TCR
repertoire as pathogenic CD4+ T cells |
[30] |
|
|
Reduced frequencies of nTreg in patients with RA |
[31] |
|
|
Tregs unable to suppress spontaneous generation of TNFα in synovial
cells of RA patients due to reduced expression of CTLA-4 and LFA-1 |
[32] |
2. |
Multiple Sclerosis (MS) |
CD4+CD25+ Treg cells/Treg-derived
exosomes from multiple sclerosis patients are inefficiently suppressive.
Circulating exosomes with significantly high miRNA let-7i in MS
patients, inhibit Treg function through an IGFR1 and TGFBR1 mechanism. |
[33-35] |
|
|
CD25+CD127low Treg development
and function are perturbed.
CD39+FoxP3+ memory Treg are
diminished in MS patients. Expression of PD-1 is high on theses Tregs in
MS, suggesting possible exhaustion and compromised function. |
[36,37] |
3. |
Systemic Lupus Erythromatosis (SLE) |
CD25+Lag3+ T cells, expressing FoxP3
and IL-17A, but not being suppressive are increased in patients with
SLE. The frequency of CD25+Lag3+
cells positively correlates with SLE disease activity. |
[38] |
4. |
Type 1 Diabetes |
Reduced suppressive function of Treg cells in
Type 1 diabetes patients possibly due to reduced CD39 expression on
memory Treg cells. |
[39] |
|
|
Differentiation and stability of Tregs is impaired in Type 1
diabetes through a miRNA-1423p dependent mechanism. |
[40] |
|
|
FoxP3 expression declines with type 1 diabetes disease progression
suggesting loss in Treg function. The rate of loss is greatest in
Peptidase inhibitor -16 or Pi16+ Treg cells |
[41] |
5. |
Malaria |
FoxP3+Treg cells increase in humans and
mice during blood stage malaria and hamper Th and Tfh-B cell
interactions. |
[42] |
|
|
Frequency of FoxP3+ Tregs declines in children
with age in high exposure malaria settings. |
[43] |
6. |
Dengue |
Treg frequencies are higher in mild cases of dengue
compared to moderate cases and healthy controls. |
[44] |
|
|
Treg frequencies in acute dengue fever are high and most of the
expanded Treg population comprises of naïve Tregs with poor suppressive
potential. |
[45] |
7. |
HIV |
HIV infected paediatric slow progressors have higher Treg
absolute numbers with a suppressive phenotype compared to rapid
progressors. |
[46] |
|
|
Depletion of
CD4+CD25hiCD62Lhi
Tregs are depleted in HIV infection and this correlates with immune
activation. |
[47] |
|
|
HIV+ elite suppressors maintain higher levels of Treg and lower
immune activation compared to progressors. |
[48] |
|
|
Frequency of PD-1+ Tregs increases in HIV and
blockade of the PD-1/PD-L1 pathway increases TGF-β and IL-10 in
CD4+CD25hiCD127loTreg
cells. |
[49] |
|
|
Individuals who do not respond to ART have fewer dysfunctional Tregs
with defects in mitochondrial function compared to healthy controls and
HIV patients who respond to ART. |
[50] |
8. |
Candida infection |
Candida albicans infection in a mouse
model drives expansion of Tregs which corresponds with increased fungal
burden. Expanded Tregs suppress Th1 and Th2 but promote pathogenic Th17
responses. |
[51, 52] |
9.
|
Leishmaniasis
|
Foxp3+IL-10+ Treg cells are enriched
in bone marrow of visceral leishmaniasis patients with high parasite
load compared to those with low parasite load.
Frequency of
CD4+CD25hiFoxP3+
Treg cells correlates with parasite load in Kala-azar patients infected
with Leishmania donovani.
|
[53, 54]
|
10. |
Tuberculosis |
While some studies have found Treg frequencies to
increase in blood and lungs of TB patients, others have found them to
remain unchanged. |
[55-61] |