Table 1 Recent studies on the effect of immune cell-derived exosomes (TXEs) on the tumor microenvironment (TME) in lung cancer

Tumor-Associated Macrophages (TAMs)

A549 cells/Vesicular cargoes

Ultracentrifugation

TEXs derived from lung tumors are capable of inducing a shift in the phenotype of M0 macrophages towards the M2 type by modifying their transcriptional and bioenergetic profiles

[82]

Tumor-Associated Macrophages (TAMs)

NCI-H1792, NCI-H1437, NCI-H2087

(Human adenocarcinoma cell lines)

miR-103a

Exosome isolation kits (Exo-ELISA)

Lung cancer-derived exosomes exposed to hypoxia boosted M2-type polarization via miR-103a transfer, which upregulated AKT and STAT3 activation and the expression of multiple immunosuppressive and pro-angiogenic markers

[83]

Tumor-Associated Macrophages (TAMs)

A549 & H23 cells

miR-21-5p

Precipitation, TEM

Exosomes originating from HMSCs, which were exposed to hypoxia prior, substantially boosted the growth, endurance, invasion, EMT, and increased the expression of miR-21-5p. This, in turn, suppressed apoptosis and increased M2 polarization of macrophages, leading to the promotion of lung cancer development

[84]

Tumor-Associated Macrophages (TAMs)

Adenocarcinoma human alveolar basal epithelial cells (A549) / Vesicular cargoes

Precipitation, TEM

Exosomes from hypoxic A549 cells increased proliferation, migration, EMT, and PKM2 expression leading to PKM2-induced M2 polarization of macrophages through the AMPK pathway resulting in tumor development, and lung metastasis

[85]

Tumor-Associated Macrophages (TAMs)

A549 cells / Vesicular cargoes

The invasion and metastasis of A549 cells are facilitated by miR-10b in exosomes released by tumor cells, which induces polarization of M2 macrophages

[86]

Cancer-associated fibroblasts (CAFs)

CAFs from NSCLC cancer tissue and NFs from para-carcinoma tissue/ miR-103a-3p

Ultra-centrifugation, TEM

CAFs produce exosomal miR-103a-3p that hinders apoptosis by targeting Bak1, which could be a promising therapeutic option for addressing cisplatin resistance in NSCLC

[87]

Cancer-associated fibroblasts (CAFs)

A549 cells

PBMC cells

Exosomal OIP5-AS1 from CAFs inhibited PBMC-induced cell apoptosis and enhanced lung cancer proliferation by decreasing miR-142-5p and increasing PD-L1

[88]

Cancer-associated fibroblasts (CAFs)

Embryonic mouse fibroblast cell line (NIH3T3) / miR-210

Ultra-centrifugation, TEM

Exosomes generated from LCs may stimulate cell reprogramming, allowing fibroblasts to differentiate into CAFS, and overexpression of exosomal miR-210 might promote angiogenesis and may trigger the expression of proangiogenic proteins via the JAK2/STAT3 signaling pathway

[89]

Myeloid-derived suppressor cells (MDSC)

95D (human lung cancer cells), H292 (lung mucoepidermoid carcinoma cells), H358 ( lung adenocarcinoma cells),

miR-21a

Ultra-centrifugation, TEM

Exosomes from lung carcinoma cells contain miR-21a which targets PDCD4 to promote the proliferation of MDSCs, accelerating tumor progression

[90]

Myeloid-derived suppressor cells (MDSC)

Human lung cancer cell lines, and mouse lung cancer cell line, Lewis LLC cell line /miR-143-3p

Ultracentrifugation and TEM

More exosomes were produced by G-MDSCs in lung cancer tissues, thereby promoting cancer progression. Upregulation of miR-143-3p in G-MDSCs-derived exosomes significantly attenuates ITM2B by binding to its 3'-untranslated region

[91]

Dendritic Cells (DCs)

LLC, A549, and Beas-2b/ MALAT1

Precipitation, (exosome extraction kit)

MALAT1 inhibition may be a promising method for treating lung cancer since it increases DC function and T cell proliferation while suppressing DC autophagy and T proliferation and differentiation in LLC-derived exosomes when MALAT1 expression is inhibited

[92]

Dendritic Cells (DCs)

A549 cells

LLC cells

Ultracentrifugation

TEXs effectively promote DC maturation and increase MHC cross-presentation, leading to a more potent tumor-specific cytotoxic T-cell response. More crucially, TEXs lower DC PD-L1 expression resulting in a down-regulated population of Tregs in vitro

[93]

Dendritic Cells (DCs)

BMDCs/EGFR gene mutation E746-A750

Ultracentrifugation

Loss of intratumoral CD8 + T lymphocytes correlates with the progression of harbouring the E746-A750 deletion mutation (EGFR-19del). Early-stage EGFR-19del-expressing LLC tumors are characterized by a low T cell density and the presence of DC with diverse morphologies

[94]

T cells

A549, PC9,95D/CircRNA-002178

Exosome Precipitation Solution kit

CircRNA-002178 might increase PD-L1 expression in cancer cells by syphoning miR-34, causing T-cell fatigue, and could serve as biomarkers for early detection of lung adenocarcinoma

[95]

T cells

Human NSCLC cell lines

Ultracentrifugation

Exosomes generated from lung cancer cells express PD-L1, which aids immunological evasion by decreasing T cell activation and encouraging tumor development. Exosomes can reduce cytokine production and induce death in CD8 + T cells, impairing immunological activity

[96]

T cells

Human NSCLC cell lines

ExoQuick Exosome Precipitation Solution kit

NSCLC cells are responsible for the majority of exosomal circUSP7 secretion, and this leads to immunosuppression in NSCLC by increasing malfunction in CD8 + T cells

[97]

Natural killer cells (NKs)

A549, Mouse NK cell line

(LNK)

ExoEasy Maxi kit precipitation lit

Modulating the expression of miR-30c could be a potential strategy to enhance NK cell-based anticancer treatments. This is suggested by its ability to increase the cytotoxicity of NK cells towards lung cancer cells through the reduction of GALNT7 and inactivation of the PI3K/AKT pathway

[98]